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DENTAL   PATHOLO 


THERAPEUTICS 


FOR  STUDENTS  AND  PRACTITIONERS 


BY 

HENRY  H.  BURCHARD,  M.D.,  D.D.S. 

LATE   SPECIAL  LECTURER    ON    DENTAL   PATHOLOGY   AND  THERAPEnTICS    IN  THE    PHILADELPHIA 

DENTAL   COLLEGE 


REVISED  BY 

OTTO  E.  INGLIS,  D.D.S. 

PROFESSOR   OF   DENTAL  PATHOLOGT   AND   THERAPEUTICS   IN  THE   PHILADELPHIA 
DENTAL   COLLEGE 


SECOND    EDITION 

ILLUSTRATED   WITH    545    ENGRAVINGS   AND  A   COLORED    PLATE 


-4- 


LEA   BROTHERS   &   CO. 
PHILADELPHIA    AND    NEW   YORK 

1904 


1.Q04 


Entered  according  to  the  Act  of  Congress,  in  the  yea-r  1904,  by 

LEA    BROTHERS    &    CO., 
in  the  Office  of  the  Librarian  of  Congress.     All  rights  reserved. 


DORNAN,     PRINTEH. 


THIS 

VOLUME 

IS   AFFECTIONATELY   DEDICATED 

TO   THE 

MEMORY    OF 

J.    FOSTER    FLAGG,    D.D.S. 

AND 

HENRY  H.  BURCHARD,  M.D.,  D.D.S. 

IN   RECOGNITION    OF  THEIR   UNSELFISH 

EFFORTS    FOR 

PROFESSIONAL    ADVANCEMENT 


Digitized  by  tine  Internet  Archive 

in  2010  witii  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/textbookofdental1904burc 


PREFACE  TO  SECOND  EDITIO^s^ 


In  re\4sing  this  work  the  Editor  has  borne  in  mind  the  original 
motive  of  its  author,  namelv,  the  production  of  a  text-book  wiiich 
may  serve  as  a  useful  basis  of  instruction  upon  a  subject  which 
students  find  difficult  to  comprehend  from  lectures  alone.  To  this 
end,  while  the  original  plan  and  arrangement  of  chapters  have  been 
in  the  main  adhered  to,  no  hesitancy  has  been  felt  in  re\-ising  the 
text,  which,  with  the  exception  of  certain  portions,  has  been  re- 
written in  order  that  new  material  might  be  inserted  in  its  proper 
place  and  bearings.  "Where  material  has  been  drawn  from  the 
work  of  others  full  credit  has  been  accorded.  The  section  on 
pharmacology  has  been  omitted,  and  in  its  stead  the  remedial 
agents  referred  to  in  the  text  have  been  completely  indexed,  so  that 
their  uses  may  be  studied  without  difficulty. 

The  Editor  desires  here  to  express  his  thanks  to  the  authors  whose 
illustrations  appear  in  the  book  and  to  the  editors  and  publishers 
of  the  various  dental  journals  and  text-books  from  which  they  have 
been  taken.    In  no  instance  has  a  request  been  denied. 

In  consideration  of  the  fact  that  acknowledgment  is  not  mani- 
fest in  the  text,  the  Editor  would  thank  the  S.  S.  WTiite  Dental  Manu- 
facturing Company,  the  Dental  Manufacturing  Company,  Limited 
(London),  P.  Blakiston,  Son  &  Company,  William  Wood  &  Com- 
pany, and  the  J.  B.  Lippincott  Company,  for  cuts  from  text-books 
published  by  them.  Thanks  are  also  due  to  Lea  Brothers  &  Com- 
pany, from  whom  the  Editor  has  received  the  most  generous  aid  and 
who  have  spared  no  pains  to  comply  with  every  desire. 

O.  E.  L 

Philadelphia.  August.  1904. 


PREFACE  TO  FIRST  EDITION. 


This  volume  is  designed  as  a  text-book  of  the  principles  and  prac- 
tice of  dental  medicine  for  the  use  of  students,  and  as  a  reference  work 
on  applied  special  pathology  and  therapeutics  for  the  use  of  dentists. 
Accepting  the  dictum  of  the  advanced  teachers  of  the  day,  the  writer 
believes  that  an  entirely  rational  system  of  dental  medicine  can  have 
but  one  basis — namely,  the  same  principles  which  underlie  general 
medical  and  surgical  practice.  The  book  represents,  therefore,  an 
attempt  at  formulating,  from  data  obtained  from  every  available 
source,  a  system  of  dental  pathology  and  therapeutics  of  which  the 
several  parts  shall  be  in  harmony  with  one  another  and  also  with  the 
several  collateral  sciences  involved.  The  impulse  prompting  the  work 
was  no  desire  to  multiply  books,  but  arose  from  a  conviction  expressed 
by  many  teachers,  that  such  a  volume  is  needed  by  students,  prac- 
titioners, and  teachers. 

The  extent  and  scope  of  references  may  be  only  partially  seen  in 
the  numerous  foot-note  references,  space  limitations  precluding  any 
exhaustive  bibliography. 

It  would  be  unjust,  however,  to  omit  this  opportunity  to  credit 
two  investigators  without  whose  researches  this  volume  would  have 
been  impossible:  Professors  G.  V.  Black  and  W.  D,  Miller,  to  whom 
frequent  and  specific  references  are  made. 

The  immense  development  of  modern  dentistry  has  brought  with 

it  a  more  rational  and  convenient  grouping  of  its  subjects.     The 

American    Text-books    of   Operative    and    Prosthetic   Dentistry   have 

already  won  acceptance,  each  in  its  own  field.    They  leave  untouched 

a  range  of  subjects  which  are  naturally  cognate,  and  hence  are  most 

advantageously  taught  in   conjunction — namely.   Dental   Pathology, 

Therapeutics,  and  Pharmacology.     The  fitness  of  this  grouping  is 

manifest. 

H.  H.  B. 

April,  1898. 


CONTENTS. 


SECTION   I. 
GENERAL   PATHOLOGY. 

CHAPTER  I. 

PAGE 

General,  Principles 17 

CHAPTER  II. 

Causes  op  Disease,  General  and  Local 26 

CHAPTER  III. 
Micro-organisms  as  Exciting  Causes  of  Disease 34 

CHAPTER  IV. 
Disturbances  of  Nutrition 50 

CHAPTER  V. 
Disturbances  of  the  Vascular  System 71 


SECTION  IL 
EMBRYOLOGY,  ANATOMY,  AND  HISTOLOGY. 

CHAPTER  VI. 

The  Development,  Anatomy,  and  Histology  of  the  Jaws  and  Teeth   .      107 

CHAPTER  VII. 
The  Surgical  Anatomy  of  the  Teeth 156 

CHAPTER  VIII. 

Dentition:  Its  Progress,  Variations,  and  Attendant  Disorders  .      .     177 

CHAPTER  IX. 

Malformations  and  Malpositions  of  the  Teeth 206 

(ix) 


X  CONTENTS. 

SECTION   III. 
AFFECTIONS  OF  THE  ENAINIEL  AND  DENTINE. 

CHAPTER  X. 

PAGE 

Abrasions,  Erosions,  and  Stains 247 

CHAPTER  XI. 
Stains  of  the  Enamel  and  Dentine 269 

CHAPTER  XII. 

Dental  Caries:  History;  Exciting  AND  Predisposing  Causes   ....     277 

CHAPTER  XIII. 

Dental  Caries  :  Pathology,  Morbid  Anatomy,  and  Clinical  History  .     292 

CHAPTER  XIV. 
Dental  Caries:  Diagnosis,  Symptoms,  and  Prognosis 323 

CHAPTER  X^\ 

Dental  Caries:  Therapeutics  and  Prophylaxis 339 


SECTION   IV. 

DISEASES  OF  THE  DENTAL  PULP. 

CHAPTER  X^^I. 
Constructive  Diseases 361 

CHAPTER  XVII. 
Destructive  Diseases  of  the  Dental  Pulp 382 

CHAPTER  XVIII. 

Methods  of  Removal  of  the  Dental  Pulp  and  Root-canal  Filling   .     419 

CHAPTER  XIX. 
Gangrene  of  the  Pulp 444 


CONTENTS.  xi 

SECTION  V. 

DISEASES  OF  THE  PERICEMENTUM. 
CHAPTER  XX. 

PAGE 

Septic  Apical  Pericementitis  (Acute) 459 

CHAPTER  XXI. 

Chronic   Septic,    Purulent,  Apical   Pericementitis  (Chronic  Apical 

Abscess) 476 

CHAPTER  XXII. 

Non-septic  Pericementitis 499 


SECTION   VI. 

PERICEMENTAL    DISEASES    BEGINNING  AT   THE    GUM 

MARGIN. 

CHAPTER  XXIII 523 

CHAPTER  XXIV. 
Salivary  and  Serumal  Calculus 533 

CHAPTER  XXV. 
Pyorrhcea  Alveolaris 550 

CHAPTER  XXVI. 
Pericemental  Abscess 579 

CHAPTER  XXVII. 
Reflex  Disorders  of  Dental  Origin 590 

CHAPTER  XXVIII. 
Infection  of  and  from  the  Mouth,  and  Sterilization 602 


DENTAL  PATHOLOGY  AND  THERAPEUTICS. 


SECTION  I. 

GENEEAL   PATHOLOGY 


CHAPTER    I. 

GENERAL    PRmCIPLES. 

General  pathology  (pathos,  disease,  and  logos,  a  discourse)  is  that 
branch  of  science  which  treats  of  the  modifications  in  function  and 
changes  in  structure  occurring  in  disease.  It  embraces  all  pathological 
processes  occurring  in  the  human  body,  and  as  many  of  these  occur 
in  and  about  the  teeth  modified  only  by  the  peculiar  anatomy  of  the 
parts,  Dental  Pathology  may  be  said  to  be  that  branch  of  dentistry 
which  treats  of  modifications  in  function  and  changes  in  structure 
occurring  in  the  diseases  of  the  teeth  and  associate  parts. 

This  being  true,  it  follows  that  the  study  of  dental  pathology  must 
be  preceded  by  a  study  of  the  general  disease  processes  which  affect 
the  tissues  of  the  body,  and  such  of  these  as  are  applicable  to  the  study 
are  known  as  the  General  Principles. 

The  word  Therapeutics  is  derived  from  the  Greek  therapeuin,  to 
take  care  of,  meaning  the  measures  adopted  to  remedy  or  remove 
the  changes  induced  by  pathological  processes. 

The  study  of  the  pathology  of  a  part  begins  with  a  study  of  its 
anatomy  and  histology,  then  naturally  follows  a  study  of  its  physiology 
and  embryology.  These  form  the  basis  from  which  degrees  of  abnor- 
mal function  and  altered  structure  may  be  judged  by  comparison 
with  similar  processes  occurring  in  other  parts  of  the  body. 

The  body  is  composed  of  cells  held  together  by  intercellular  sub- 
stance. These  cells  are  the  essential  functionating  parts  of  the  organ- 
ism; each  cell  is  composed  of  a  small  mass  of  protoplasm  containing 

2 


18  GENERAL  PATHOLOGY. 

in  nearly  all  cases  a  nucleus,  and  has  a  form  adapted  to  its  environ- 
ment and  function.  The  exact  chemical  composition  of  protoplasm 
is  unknown  and  efforts  at  analysis  destroy  its  peculiar  property  as  a  sub- 
stance exliibiting  a  sequence  of  phenomena  called  life.  It  is  a  viscid 
substance  composed  physically  of  a  network  containing  a  slightly 
more  fluid  substance.^  Chemically  it  is  70  per  cent,  water  containing 
a  collection  of  proteids  and  differs  as  to  these  in  the  different  classes 
of  cells.  Proteids  are  but  imperfectly  understood,  but  are  known  to 
consist  essentially  of  carbon,  hydrogen,  oxj'gen,  and  nitrogen,  com- 
bined with  sulphur  and  other  varying  elements  in  enormous  molecules 
approximately  represented  by  the  formula  C^ooH3^(,Oi2oN.oS.-  The 
study  of  the  properties  of  cell  protoplasm  may  be  made  by  observing 
in  sihi  the  action  of  living  cells  under  normal  conditions  and  when 
subjected  to  artificial  stimuli,  and  by  observing  the  action  of  free  single 
cells  such  as  an  amoeba  under  like  conditions. 

If  a  drop  of  water  be  taken  from  the  sides  or  bottom  of  an  aquarium, 
placed  on  a  slide  and  covered  with  a  cover-glass,  and  then  placed  under 
a  microscope  with,  first,  a  \"  objective,  there  will  be  noted  at  some 
portion  of  the  fluid  a  small  transparent  mass  having 
the  appearance  of  a  colorless  fragment  of  jelly;  this 
is  an  amoeba.  The  outline  of  the  mass  may  have 
almost  any  form.  At  some  portion  there  will  be  a 
defined  and  easily  distinguished  spot,  the  nucleus  ; 
at  another  point  a  vesicle  is  seen;  the  body  of  the 
amoeba  appears  to  contain  numbers  of  fine  granules. 
The  nucleus  appears  more  markedly  granular  than 
the  body  of  the  amoeba.     If  kept  under  observation. 

Changes  of  form  in       ,  '    i  -n    i  i  •  t 

an  amoeba:  pp,  pseu-  the  amoeba  Will  06  sccu  to  chaugc  its  outlmcs;  at 
dopodia;   V,  vesicle;   ^^^  ^^  morc,  and  it  may  be  in  several  places,  pro- 

N,  nucleus.  ,         .  ,  r  '    r 

jections  like  blunt  arms  or  feet  are  seen  to  be  ex- 
tending from  the  amoeba  (Fig.  1).  On  account  of  their  appearance 
they  are  called  by  the  physiologist  pseudopodia,  from  pseiido,  false,  and 
'pous,  a  foot — false  feet.  These  changes  of  form  are  much  varied 
(Fig.  2).  The  cell  has,  therefore,  the  property  of  altering  its  form — 
i.  e.,  it  has  contractility.  If  the  temperature  of  the  slide  be  raised, 
the  movements  of  the  cell  become  more  rapid,  and  if  raised  to  a  tem- 
perature of  55°  C.  the  cell  contracts  in  a  round  lump;  it  responds  to 
stimuli,  and  has  therefore  the  property  of  irritability. 

*  1  Kirke's  Physiology.  -  Schofield,  Elementary  Physiology. 


GENERAL  PRINCIPLES. 


19 


^Mien  certain  solid  substances  contained  in  the  water  come  in  con- 
tact with  the  amoeba,  the  latter  is  seen  to  flow  around  and  eno-ulf 


Fig.  2. 


AmcEboid  movement  of  a  white  blood  corpuscle  of  man  ;  various  phases  of  movement.    (Klein.) 

them;  as  is  shown  in  Figs.  3  and  4,  where  the  analogue  of  an  amoeba, 
a  leukocyte,  has  taken  in  bacteria  (phagocytosis).     After  a  time  the 

Fig.  3.  Fig.  i. 


Fig.  3. — Leukocyte  of  a  frog  from  the  neighborhood  of  a  piece  of  the  lung  of  a  mouse  infected 
■with  anthrax,  about  forty-two  hours  after  the  piece  of  lung  had  been  placed  under  the  skin  of 
the  frog's  back.  The  leukocyte  is  in  the  act  of  eating  up  an  anthrax  bacillus.  (Brunton.  aft«r 
Metschnikoff.) 

Fig.  4.— The  same  leukocyte  a  few  minutes  later,  after  it  has  completely  enveloped  the 
bacillus.     (Brunton,  after  Metschnikoff.; 

ingested  body  is  found  to  have  disappeared;  it  has  been  digested. 
E\ddently  the  cell  must  produce  a  substance  capable  of  dissoh-ing 


Forms  assumed  by  a  nucleus  in  dividing:  a,  resting  nucleus;  5,  skein-form,  open  stage; 
C,  wreath-form;  d,  aster,  or  star-form;  e,  equatorial  stage  of  division;  /,  separation  more 
advanced;  g  and  h,  star  and  wreath  forms  of  daughter-nuclei.  (Reduced  from  Flemming's 
drawings  in  the  Arch.  f.  Mik.  Anat.) 

some  foreign  substances — i.  e.,  it  has  the  function  of  secretion.  More 
than  this,  the  amoeba  does  not  take  in  substances  indiscriminately; 
some  it  rejects. 


20  GENERAL  PATHOLOGY 

If  the  observations  are  continued,  it  will  be  noticed  that  changes 
occur  in  the  nucleus  of  the  cell.  A  series  of  alterations  in  its  figure 
are  noted,  as  shown  in  Fig.  5.  Two  nuclei  are  formed,  and  soon  the 
body  of  the  cell  divides  and  two  cells  appear — the  amoeba  has  repro- 
duced itself.  This  primitive  cell  has,  therefore,  the  properties  of  irrita- 
bility, contractility,  secretion  and  excretion  (as  will  be  seen  in  later 
studies),  and  reproduction;  moreover,  it  responds  to  stimuli,  as  seen  on 
warming  the  stage. 

If  the  stage  be  cooled,  the  movements  of  the  protoplasm  are  less- 
ened, and  when  foreign  substances  come  in  contact  with  the  cell  it  fails 
to  encompass  them — its  irritability  and  contractility  are  lessened. 

It  is  noted  that  some  simple  cells  are  attracted  and  stimulated  by 
light;  others  are  repelled  by  it. 

If  a  mild  induction  (interrupted)  current  be  passed  through  the 
water  in  which  the  amoeba  is,^  the  movements  of  the  cells  are  checked; 
if  a  strong  current  be  passed,  the  cell  contracts  sharply.  If  a  galvanic 
(constant)  current  be  passed,  movement  at  first  ceases,  but  pseudo- 
podia  are  extruded  toward  the  cathode  and  the  cell  crawls  toward 
that  pole. 

The  cell  responds  to  mechanical  stimuli,  such  as  violent  shaking, 
by  contraction.- 

If  substances  such  as  ether  or  chloroform  are  added  to  the  fluid,  the 
irritability  of  the  cell  is  so  lessened  that  it  does  not  respond  to  stimuli. 

If  the  supply  of  oxygen  be  cut  off,  or  if  carbon  dioxide  be  admitted 
to  the  fluid,  movement  ceases  and  the  cell  remains  contracted. 

These  examples  serve  to  illustrate  that  protoplasm  responds  to 
stimuli  of  physical  and  chemical  nature,  and  that  its  functions  may  be 
altered  by  substances  which  are  brought  in  contact  with  it.  Upon  these 
facts  depends  the  practice  of  therapeutics. 

A  living  organism,  it  will  be  seen,  has  a  certain  degree  of  action 
and  function.  The  general  average  of  its  action  and  function  is  spoken 
of  as  a  condition  of  health.  "Wlien,  from  any  cause,  the  functions  are 
raised  or  lowered  from  the  general  average,  a  condition  of  disease 
exists. 

Stimulation.  Certain  agencies  applied  to  the  cell  increase  its 
acti\'ity;  this  is  called  stimulation.  The  movements  of  the  cell  become 
more  rapid,  food  particles  are  taken  in  more  rapidly  and  disappear 
more  quickly;  irritability,  contractility,  and  secretion  are  increased. 

1  O.  Hertwig,  The  Cell.  -  Ibid. 


GENERAL  PRINCIPLES.  21 

The  cell  subdivides,  or  reproduces  more  quickly.  Increase  the  stimu- 
lation, and  the  vital  activity  becomes  fretful;  in  some  cases  cell  division 
is  incomplete — the  nucleus  divides,  but  not  the  cell  body.  Increase 
the  stimulation  beyond  this  degree,  and  the  wearied  cell  ceases  its 
movements — refuses  to  respond;  is  paralyzed  by  overwork. 

Sedation.  If  the  conditions  be  reversed;  if,  instead  of  applying  a 
stimulus  to  the  cell,  an  opposite  influence  be  introduced,  the  phenomena 
are  reversed. 

If  the  temperature  be  reduced,  the  movements  of  the  cell  become 
sluggish;  the  body  changes  its  form  more  slowly  and  less  extensively — 
i.  e.,  contractility  is  lessened;  particles  taken  into  the  cell  remain 
apparently  unchanged;  irritability,  secretion  and  excretion  are  less- 
ened; and,  furthermore,  reproduction  does  not  occur  nearly  so  rapidly 
— that  is,  the  cell  in  contact  with  sedative  influences  has  all  of  its 
activities  lessened. 

There  are  two  great  classes  of  influences,  then,  which  affect  the 
vitality  of  cells:  stimulation,  which,  if  continued  long  enough,  leads 
to  death  through  overwork;  and  sedation,  which,  if  continued,  para- 
lyzes all  of  the  energies  of  the  cell — it  is  starved  to  death. 

Every  cell  has  a  range  of  resistance  to  these  influences  which  tend 
to  destroy  it,  which  is  fitly  termed  the  resistance  of  vitality.  Disease 
itself  is  some  alteration  in  any  one  or  more  of  these  several  cell-proper- 
ties, of  irritability,  contractility,  growth,  secretion,  maintenance,  or 
reproduction.  If  any  one  of  these  properties  is  not  exliibited,  it  is 
said  that  the  cell  is  diseased. 

If  a  brood  of  cells  derived  from  one  parent  be  examined,  some  will 
be  seen  to  grow  more  rapidly  than  others,  their  movements  are  more 
rapid  and  they  reproduce  more  quickly;  others  have  sluggish  func- 
tions and  movements. 

The  cell  lives  its  cycle  and  reproduces,  and  the  parent  is  no  more, 
the  life  being  continued  in  the  offspring. 

The  life  and  properties  of  this  small  mass  of  protoplasm  represent 
in  miniature  the  primitive  functions  and  life  of  the  highest  animals. 

The  contractility  is  represented  in  the  motive  apparatus  of  the  higher 
animals. 

The  reception,  engulfing,  and  dissolving,  or  casting  out,  bodies  with 
which  the  amoeba  is  brought  in  contact  correspond  in  the  higher  animals 
with  the  digestive  apparatus  and  process  and  the  excretory  function. 

The  highly  evolved  irritability  is  represented  in  the  nervous  system 
of  the  higher  animals. 


22  GENERAL  PATHOLOGY. 

The  movements  occurring  in  and  about  the  vacuole  are  the  pro- 
genitors of  the  circulatory  apparatus  and  all  of  its  adjunct  organs. 

If  the  irritability  of  a  simple  cell  be  increased  or  diminished,  it 
corresponds  with  a  disease  of  the  nervous  system,  and  so  with  the 
other  functions. 

Certain  collections  of  cells  are  found  in  which  one  function  is  active, 
the  others  in  abeyance;  thus,  large  colonies  of  cells  exist  in  which 
contractility  is  the  dominant  property  noted;  these  are  muscle  cells. 
Others  have  but  the  property  of  irritability;  these  are  nerve  cells. 
Still  others  develop  peculiar  chemical  functions,  and  become  glandular 
or  secretory  cells.  Such  collections  of  cells  are  known  as  tissues.  These 
special  cell  colonies  or  tissues  are  built  together  into  defined  masses  for 
the  performance  of  their  specialized  functions.  In  the  development  of 
these  masses,  means  of  holding  and  maintaining  the  cells  in  definite 
mass  forms  and  provisions  for  their  food  supply  and  waste-removing 
apparatus  are  provided  in  what  are  called  the  connective  tissues,  bind- 
ing the  cells  in  definite  forms  and  transmitting  their  vascular  supply 
(food-  and  waste-carrier).  When  thus  bound  together  the  tissues  are 
said  to  form  organs. 

"\Miile  all  tissues  are  capable  of  analysis  into  cells  and  intercellular 
substance,  a  more  practical  view  may  resolve  the  tissues  into  (1)  func- 
tional cells;  (2)  a  supporting  intercellular  substance; '(3)  intercellular 
spaces  in  which  flows  the  Ijnnph  derived  from  the  blood;  (4)  the  chan- 
nels of  circulation  and  conductors  of  nervous  impulses — i.  e.,  arteries, 
capillaries,  veins,  lymphatics,  and  nerves.  The  arteries  bring  to  the 
tissues  the  blood  freighted  with  oxygen  and  nutrient  material.  As  it 
passes  through  the  capillaries  a  portion  of  the  blood  plasma,  under 
arterial  pressure  and  osmotic  force,  passes  into  the  intercellular  spaces 
into  contact  with  the  cells.    This  exuded  fluid  is  now  called  lymph. 

Stated  in  general  terms  the  food  materials  contained  in  arterial 
blood  and  furnished  to  the  tissues  by  way  of  the  lymph  are :  water, 
proteids,  glucose,  fats,  inorganic  salts,  and  oxygen.  From  this  store 
the  cells  take  what  they  require  and  within  themselves  they  elaborate 
substances  essential  to  their  growth  and  maintenance  as  masses  of 
functionating  protoplasm,  and  as  the  protoplasm  is  of  more  complex 
composition  than  the  majority  of  food  elements,  they  are  said  to  form 
from  simple  compounds  substances  of  a  higher  degree  of  complexity 
(anabolism).  From  their  substance  they  eject  into  the  lymph  stream 
such  waste  products  as  result  from  the  breaking  down  of  the  previously 
formed  protoplasm  (catabolism).     "There  is  reason  to  believe  that 


GENERAL  PRINCIPLES.  23 

cell  protoplasm  as  it  becomes  efiPete  takes  up  oxygen  and  splits  into 
a  nitrogenous  molecule,  which  is  the  first  stage  in  the  formation  of 
urea  and  a  non-nitrogenous  molecule  which  forms  fat."^  In  the  pro- 
cess of  healthy  nutrition  these  products  of  the  metabolism  of  the  cells 
are  still  further  elaborated  and  then  removed. 

The  exact  nature  of  the  chemical  changes  occurring  in  cells  is  not 
known,  and  there  is  evidence  that  changes  occur  in  the  cell  waste 
either  in  the  blood  or  in  various  organs  of  the  body.  Wliile  then  the 
bodily  ejecta  contain  substances  fairly  constant  in  composition,  they 
are  held  to  represent  elaborations  of  cell  waste  rather  than  actual  cell 
ejecta.  For  example,  urea  is  pretty  certainly  derived  from  muscular 
tissue,  yet  is  nearly  absent  in  muscle  and  is  supposed  to  be  synthe- 
sized from  ammonium  carbonate  and  water  in  the  liver.^  Lactic 
acid  and  ammonium  carbonate  have  been  experimentally  shown  to 
be  probably  combined  into  uric  acid  in  the  liver.'^  The  cell  waste 
is  carried  by  the  lymph  into  the  lymphatics  connecting  with  the  inter- 
cellular spaces.  Thence  it  is  delivered  by  way  of  the  venous  system 
to  the  circulation  for  further  elaboration  and  elimination  from  the 
body.  Any  interference  with  such  elaboration  or  elimination  must 
of  necessity  result  in  a  retention  of  waste  products  within  the  system. 

Cell  metabolism  is  a  chemical  change  and  is  therefore  accompanied 
by  heat  production.  Energy  is  stored  up  in  the  cell  as  latent  force 
capable  of  liberation  under  stimulus,  which  force  is  expressed  in  various 
forms  of  functional  activity — i.  e.,  contractility  in  muscular  tissue, 
irritability  and  mentality  in  nervous  tissue,  secretion  in  the  various 
secretory  glands,  eliminative  selection  in  the  various  excretory  organs, 
etc.  Cells  after  a  period  of  activity  undergo  degenerative  processes 
and  are  removed  or  reproduce  by  the  process  of  mitosis  (Fig.  5). 

The  life  conditions  of  cells  are  necessarily  those  under  which  they 
best  perform  these  functions  without  exhaustion,  and  are  the  follow- 
ing: 1,  A  proper  food  supply,  including  water  and  oxygen.  2.  A 
proper  temperature.  3.  A  proper  removal  of  waste  products.  4. 
Possibly  a  proper  innervation.  Any  interference  with  these  condi- 
tions, which  may  be  termed  the  normal  physiological  conditions,  results 
in  a  morbid  process  of  physiology  or  pathology  in  its  limited  sense. 
With  such  interference  disease  may  be  said  to  begin.  The  definition 
of  disease  as  an  alteration  of  nutrition  is  therefore  appropriate.  For 
this  reason  the  proximate  exciting  causes  of  disease  are  classed  as 

1  Green,  Pathology  and  Morbid  Anatomy,  ninth  edition,  p.  47. 

2  Schroder,  Kirke's  Physiology.  ^  Ibid. 


24  GENERAL  PATHOLOGY. 

(1)  abnormal  food  supply;  (2)  abnormal  waste  removal;  (3)  abnormal 
physical  condition;  (4)  abnormal  nerve  supply. 

The  morbid  physiology  results  in  morbid  products  or  in  retained 
normal  products  and  an  altered  cell  function.  When  pronounced 
this  is  spoken  of  as  Functional  Disease,  though  it  may  be  said  to 
be  in  existence  even  if  discomfort  be  not  produced.  Sooner  or  later 
an  abnormal  change  in  the  histological  characteristics  of  the  cells 
or  intercellular  substance  may  occur  which  has  been  referred  to  as 
Morbid  Histology.^  As  definite  microscopic  and  often  macroscopic 
appearances  are  associated  with  certain  diseased  conditions,  these 
are  referred  to  as  the  Morbid  Anatomy  of  a  Disease.  The  phenomena 
associated  with  a  disease  are  called  its  Semeiology  (semeion,  a  mark 
or  sign)  or  Symptomatology,  and  are  either  described  by  the  patient 
as  sensations  or  pains  of  varied  character  or  situation  (Subjective 
Symptoms),  or  may  be  noted  by  normal  or  aided  vision,  by  physical 
examination,  or  chemical  analysis  (Objective  Symptoms).  That 
which  excites  a  disease  or  promotes  the  action  of  the  excitation  is 
called  a  Disease  Cause.  The  study  of  disease  causes  is  Etiology  {aetios, 
a  cause,  and  logos).  It  is  noted  that  diseases  having  a  fairly  defined 
pathology  and  morbid  anatomy  have  from  their  beginning  to  ending 
tolerably  constant  phenomena;  they  have  each  a  natural  history; 
this  is  called  the  Clinical  History  of  a  Disease. 

The  study  of  the  origin  and  development  of  a  disease  together  is 
known  as  its  Pathogenesis  (/pathos,  disease;  genesis,  birth).  Through 
the  study  of  the  characteristic  symptoms  of  diseases,  as  well  as  those 
common  to  several  diseases,  a  particular  disease  may  be  distinguished. 
This  is  called  Diagnosis  (dia,  a  part;  gnosis  knowledge)— Direct  Diag- 
nosis when  there  is  no  question  as  to  the  symptoms,  Differential  Diag- 
nosis when  several  diseases  are  possible  and  the  characteristics  of 
one  are  considered  as  more  pronounced.  Under  certain  circumstances 
a  disease  may  be  inferred  to  be  present  by  excluding  all  other  possible 
conditions  (Diagnosis  by  Exclusion) .  In  the  course  of  a  disease  experi- 
ence has  shown  that  certain  signs  and  symptoms  are  apt  to  be  followed 
by  good  or  ill  results  as  the  case  may  be.  By  these  signs  and  symp- 
toms it  may  be  foretold  with  some  degree  of  assurance  what  will  be 
the  probable  outcome  of  the  disease.  The  inference  based  upon  these 
symptoms  is  known  as  the  Prognosis  {pro,  before;  gnosis,  knowledge). 
The  care  of  or  treatment  of  a  disease  is  its  Therapeutics.    This  involves 

1  Green,  Pathology  and  Moi-bid  Anatomy. 


GENERAL  PRINCIPLES.  25 

a  knowledge  of  remedies  applicable,  known  as  the  Materia  Medica. 
When  applied  upon  the  basis  of  a  scientific  study  of  the  pathogenesis, 
clinical  history,  and  prognosis  of  disease  and  a  parallel  knowledge 
of  the  physiological  action  of  drugs  and  of  other  remedies,  the  treat- 
ment is  known  as  Rational  Therapeutics.  When  the  treatment  is 
based  upon  the  known  good  effects  of  a  remedy  in  a  certain  disease, 
and  not  upon  its  physiological  action,  it  is  known  as  Empirical  Thera- 
peutics. 

The  pathogenesis  of  a  disease  being  known,  intelligent  efforts  may 
be  exerted  for  its  prevention.  The  causes  may  be  removed  or  neutral- 
ized before  they  have  an  opportunity  to  act;  this  is  Prophylaxis.  The 
science  of  prevention  of  disease  upon  the  broad  basis  of  a  knowledge 
of  and  observance  of  laws  of  health  is  Hygiene. 

It  will  be  seen  that  a  knowledge  of  special  pathology  can  only  be 
obtained  from  (1)  a  knowledge  of  pathology  in  general  or  at  least  of 
those  principles  of  general  pathology  which  underlie  all  disease  pro- 
cesses; (2)  a  knowledge  of  the  local  anatomy  and  histology;  (3)  a  loiowl- 
edge  of  local  embryology  and  physiology;  (4)  a  study  of  local  pathology 
and  morbid  anatomy.  To  this  must  be  added  a  study  of  materia  medica 
and  special  therapeutics. 


CHAPTER   II. 
CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL. 

A  DISEASE  cause  may  be  defined  as  any  influence  of  whatsoever 
nature  which  is  capable  of  disturbing  the  nutritive  balance  of  any 
portion  of  the  body.  The  branch  of  study  which  deals  with  the  causes 
of  disease  is  called  Etiology. 

The  causes  of  disease  are  classed  as  Exciting  and  Predisposing. 
These  are  each  divisible  into  Extrinsic,  originating  from  without,  and 
Intrinsic,  originating  within  the  bodv. 

EXCITING  CAUSES   OF  DISEASE. 

These  are  influences,  either  extrinsic  or  intrinsic,  which  are  com- 
petent to  suddenly  or  gradually  interfere  with  the  nutrition  of  the 
cells  of  a  part  or  with  the  general  nutrition  of  cells.  These  influences 
are  very  numerous,  but  may  be  grouped  according  to  their  action 
under  a  few  convenient  headings:  1.  Abnormal  Food  Supply.  2. 
Abnormal  Waste  Removal.  3.  Abnormal  Physical  Conditions.  4. 
Abnormal  Nerve  Supply. 

These  are  termed  the  Proximate  Exciting  Causes,  as  their  effects 
are  immediately  exerted  upon  the  cells.  Other  causes  may  be  back 
of  these  and  are  spoken  of  as  Primary  Causes— e.  g.,  tuberculosis 
of  the  lungs  (primary)  may  cause  insufficient  oxygenation  of  the  blood 
which  constitutes  an  abnormal  food  supply  (proximate). 

Abnormal  Food  Supply.  By  abnormal  food  supply  is  meant  an 
altered  quantity  or  quality  of  nutritive  elements  delivered  to  the  cells 
either  of  a  part  or  of  the  entire  body.  The  primary  causes  of  this  may 
exist  as  disturbances  or  faults  in  any  of  the  food-elaborating  organs, 
the  lungs,  the  eliminating  organs,  or  the  oxygen  carriers  of  the  blood 
may  exist  in  lessened  numbers.  In  the  first  case  the  c|uality  or  quan- 
tity of  nutritive  material  is  impaired,  in  the  second  case  oxygenation 
is  insufficient,  and  in  the  third  case  material  injurious  to  cells  are 
retained  in  the  body  and  are  again  presented  as  food  to  the  cells,  acting 
as  poisons.    Poisonous  or  even  non-poisonous  drugs,  and  the  products 


EXCITING  CAUSES  OF  DISEASE.  27 

of  bacterial  action,  whether  absorbed  from  the  intestines  or  from  foci 
of  infection,  have  all  more  or  less  deleterious  action  upon  cell  proto- 
plasm, violent  if  entering  the  blood  in  quantity,  chronic  if  entering 
continuously. 

In  ansemia  the  red  corpuscles  are  reduced  in  number,  hence  less 
oxygen  is  carried  to  the  tissues. 

Faults  in  the  circulatory  apparatus  interfering  with  the  circulation 
generally  cause  an  interference  with  general  nutrition,  while  local 
disturbances  of  the  circulation  from  any  cause  disturb  the  relations 
of  the  blood  supply  to  the  nutrition  of  a  part.  Thus  the  fresh  blood 
supply  may  be  excessive,  as  in  the  milder  form  of  arterial  hyperaemia, 
or  deficient,  as  in  venous  hyperaemia  and  inflammation. 

Abnormal  Waste  Removal.  Abnormal  waste  removal  is  ordinarily 
included  under  the  heading  of  abnormal  food  supply,  and  it  is  evident 
that  retention  of  waste  in  the  blood  causes  the  presentation  to  cells 
of  an  abnormal  food  or  poison.  In  local  conditions  such  as  venous 
hyperaemia  and  inflammation  the  stasis  causing  waste  retention  pre- 
vents the  access  of  a  fresh  food  supply  as  well.  In  kidney  disease 
the  substances  ordinarily  physiologically  eliminated  by  the  kidneys 
are  retained  in  the  blood  and  act  as  poisons  to  cell  protoplasm  gen- 
erally. 

Abnormal  Physical  Conditions.  This  class  of  disease  causes  in- 
cludes all  injuries  due  to  any  of  the  physical  or  chemical  forces :  Trau- 
matic injuries,  such  as  cuts,  bruises,  surgical  openings,  etc. :  Mechanical 
causes,  such  as  compressions,  obstructions  to  ducts  or  the  natural  out- 
lets of  the  body,  faults  in  the  circulatory  mechanism,  stoppages  in 
the  arteries  or  veins,  abnormal  temperature,  burns,  freezing,  etc.: 
Irritations  of  various  sorts,  such  as  those  due  to  mustard,  arsenic,  etc. 
Chemical  causes,  such  as  the  action  of  acids  or  caustics,  and  the  local 
effects  of  micro-organisms  may  all  be  classified  under  this  heading. 
The  disturbance  is  due  to  either  a  direct  destruction  of  the  life  of  the 
cells  or  an  interference  with  the  circulation  in  a  part. 

Abnormal  Nerve  Supply.  It  is  known  that  division  of,  injury  to, 
or  disease  of  certain  nerves  causes  trophic  or  nutritional  changes  in 
the  part  to  which  they  are  supplied.  \Vhether  the  nutrition  of  the 
parts  is  controlled  by  special  trophic  nerve  fibres  has  not  been  demon- 
strated. Halliburton,^  in  support  of  the  trophic  influence  of  nerves, 
instances  that  when  the  fifth  nerve  (sensory)  is  divided  beyond  the 

^  Kirke's  Physiology. 


28  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL. 

Gasserian  ganglion,  ulceration  of  the  cornea  results;  while  if  the 
seventh  nerve  (motor)  be  divided  or  paralyzed,  the  eyeball  is  equally 
exposed  to  irritants,  yet  does  not  ulcerate.  He  also  instances  that  divi- 
sion of  the  vagi  produces  fatty  degeneration  of  the  heart. 

Wliile  admitting  the  lack  of  anatomical  proof,  he  regards  the  tro- 
phic influence  of  nerves  upon  parts  to  be  unexplainable  upon  the 
ground  taken  by  others,  that  all  apparently  trophic  changes  are  due 
to  disturbances  of  the  vasomotor  nerves  controlling  the  calibre  of 
vessels.  According  to  these  other  observers  degrees  of  dilatation  are 
produced  which  modify  the  amount  of  blood  delivered  to  a  part  and 
thus  modify  its  nutrition. 

Effects  are  produced  upon  nutrition  by  causes  which  can  act  only 
through  the  nervous  system — e.  g.,  the  effect  of  anxiety  upon  appetite 
and  digestion.  The  interdependence  of  these  classes  of  causes  is  almost 
self-evident;  for  example,  constant  suppuration  at  a  focus  of  infec- 
tion (abnormal  physical  condition)  may  induce  a  toxaemia  (abnormal 
food  supply)  which  may  be  responsible  for  kidney  or  other  disease 
(abnormal  physical  condition) ,  resulting  in  the  retention  of  waste  prod- 
ucts in  the  blood  (abnormal  waste  removal  or  food  supply)  which 
has  a  vicious  result  upon  all  metabolism,  including  that  of  the  nervous 
system,  inducing  in  turn  an  abnormal  nerve  supply  and  lessening 
resistance  even  in  the  tissues  about  the  original  focus  of  infection. 
Such  a  train  of  events  is  known  as  the  establishment  of  a  vicious  circle^ 


PREDISPOSING  CAUSES  OF   DISEASE. 

A  predisposing  cause  of  disease  is  one  which  influences  the  cells  or 
juices  of  the  body  or  part  in  such  a  manner  as  to  lessen  the  resistance 
to  the  action  of  the  exciting  causes  of  disease. 

It  must  be  considered  that  a  predisposition  or  lessened  resistance 
is  in  itself  a  condition  of  disease,  not  recognizable  perhaps,  yet  a  de- 
parture from  the  standard  of  the  best  health  of  an  individual  or  part. 
For  the  most  part  predisposition  is  regarded  in  its  relation  to  the 
extrinsic  causes  of  disease,  such  as  bacterial  influences.  Predisposition 
is  either  general  or  local. 

General  Predisposition. 

This  is  either  (1)  a  natural  or  inherent  lack  of  resistance  to  infec- 
tious or  non-infectious  diseases,  or  (2)  an  acquired  lack  of  resistance 


PREDISPOSING  CAUSES  OF  DISEASE.  29 

to  infectious  or  non-infectious  diseases.  The  human  race  in  general 
is  naturally  predisposed  to  many  infectious  diseases,  such  as  tuber- 
<?ulosis,  cholera,  malaria,  measles,  smallpox,  typhoid  fever,  scarlet 
fever,  and  syphilis.^  AATien  a  person  is  exposed  to  the  disease  and 
contracts  it  he  is  said  to  be  predisposed  to  it.  If  he  does  not  contract 
it  his  system  is  immune  either  temporarily  or  permanently.  (See  Im- 
munity.) This  immunity  is  ordinarily  operative  when  the  individual 
is  in  the  best  state  of  health,  and  when  a  departure  from  this  standard 
is  brought  about  by  any  cause  exciting  infective  causes  may  then  act. 
This  is  accjuired  predisposition.  Some  indi^dduals  have  a  natural  or 
congenital  lessened  resistance  to  external  influences  of  a  non-infec- 
tious character,  such  as  heat  or  cold,  mental  effort  or  nervous  irrita- 
tions of  a  degree  ordinarily  borne  by  the  great  majority  of  indiAiduals. 
This  may  also  be  acquired,  as,  for  example,  by  extreme  subjection  to 
the  above  or  other  enervating  causes.  An  inherited  predisposition 
to  such  diseases  as  insanity,  cancer,  or  gout  may  exist. 

Some  persons  cannot  bear  certain  kinds  of  food  without  illness  or 
react  strongly  to  small  doses  of  drugs.  This  is  called  an  idiosyncrasy 
and  may  be  either  congenital  or  acquired. 

The  predisposing  causes  capable  of  producing  a  lessened  resist- 
ance may  be  grouped  under  a  few  headings. 

Sex  as  an  Intrinsic  Predisposing  Cause.  In  this  connection  the 
influence  of  sex  upon  predisposition  to  disease  must  be  considered. 
"VMiile  the  general  resistive  power  of  the  bodies  of  both  sexes  may  be 
regarded  as  practically  equal  under  similar  conditions,  yet  the  anatom- 
ical structures  and  physiology  of  each  sex  have  an  influence  upon  predis- 
position to  certain  diseases.  Aside  from  the  diseases  peculiar  to  sex, 
on  account  of  their  peculiar  organs,  each  sex  exhibits  predispositions 
to  diseases  which  the  other  sex  escapes;  for  many  of  these  the  habits 
of  life  furnish  an  explanation,  for  others  an  explanation  is  not  avail- 
able. For  example,  while  women  are  predisposed  to  functional  and 
emotional  disturbances  of  the  nervous  system,  such  as  hysteria,  they 
are  almost  exempt  from  such  structural  nervous  diseases  as  locomotor 
ataxia  and  general  sclerosis.  Males  are  much  more  subject  to  haemo- 
philia than  women. 

Age.  During  the  first  two  vears  after  birth  the  nervous  svstem 
and  the  appendages  of  the  alimentary  canal  are  developing,  and 
improper  feeding,  difficult  teething,  or  other  infiuences  readily  act 
as  exciting  causes  of  alimentary  or  nervous  disturbances. 

'  Ziegler.  General  Pathology. 


30  CAUSES  OF  DISEASE,  GENERAL  AXD  LOCAL. 

Later  children  are  subject  to  acute  infectious  diseases,  especially 
tuberculosis,  diphtheria,  and  the  eruptive  fevers.  At  adolescence  other 
predispositions  occur,  notably  chlorosis  in  young  girls.  Later  come 
the  diseases  of  early  maturity,  such  as  typhoid  fever,  pulmonary- 
tuberculosis,  and  to  a  degree  dental  caries. 

In  old  age  or  middle  life  occur  arterial  and  other  degenerations 
and  diseases  consequent  upon  them  or  upon  overstimulation  of  organs 
or  tissues. 

Temperament.  Temperament  is  the  peculiar  congenital  consti- 
tution of  an  individual  imparting  certain  physical  characteristics  and 
certain  natural  tendencies. 

There  are  four  basal  temperaments.  The  sanguine  is  that  in  which 
individuals  are  decidedly  inclined  to  the  blonde  type  with  evidence 
of  an  abundance  of  the  nutritive  fluid,  the  blood — i.  e.,  the  vascular 
system  is  said  to  dominate  the  other  functions  of  the  body.  Such  are 
predisposed  to  acute  pulmonary  and  cardiac  diseases  and  inflammatory 
disturbances  of  serious  import.  The  mental  characteristics  of  this 
temperament  are  hopefulness,  cheerfulness,  and  solidity  but  floridity  of 
mental  endowments.  The  recuperative  power  is  good.  The  bilious 
temperament  is  characterized  by  a  decided  inclination  to  the  brunette 
type,  with  evidence  of  a  domination  of  other  functions  by  the  liver. 
There  is  a  tendency  to  hepatic  and  digestive  derangements  and 
despondency;  at  the  same  time  there  is  possessed  great  physical  and 
mental  strength,  together  with  a  reliable  recuperative  power. 

The  nervous  temperament  is  indicated  by  the  smallness  and  delicacy 
of  frame  and  the  quickness  of  motion  and  perception,  evidencing  a 
domination  by  the  nervous  system  to  diseases  of  which  such  tempera- 
ment predisposes. 

The  lymphatic  temperament  is  indicated  by  bulk,  pallor,  and  flac- 
cidity  of  tissue,  a  colorlessness  of  temperament,  indicating  an  inherent 
feebleness.  There  is  a  tendency  to  serious  chronic  conditions.  This 
temperament  is  accompanied  by  poor  recuperative  force. 

There  are  no  individuals  of  pure  basal  temperament,  so  that  the 
nearest  approach  is  a  dual  temperament  such  as  the  bilio-sanguine, 
in  which  the  characteristics  of  the  sanguine  predominate  strongly 
modified  by  those  of  the  bilious  temperament.  In  like  manner  the 
sanguo-nervous,  nervo-lymphatic,  and  other  classes,  twelve  in  number, 
are  recognized  as  having  typical  representatives  in  each  community. 
A  third  or  ternary  classification  is  possible — e.  g.,  sanguo-nervo- 
bilious.     It  will  be  seen  that  temperament  has  a  distinct  relation  to 


PREDISPOSING  CAUSES  OF  DISEASE.  31 

the  vital  resistance  normally  implanted  in  an  individual,  and  there- 
fore may  to  a  certain  extent  be  counted  upon  in  a  prognosis.  Tem- 
perament is  a  predisposing  cause  probably  only  in  so  far  as  it  intro- 
duces a  natural  general  lack  of  resistance  to  disease,  or  irresistibly 
drives  an  individual  into  certain  habits  of  life  which  may  become  the 
cause  of  a  lessened  resistance. 

Heredity.  Certain  diseases  exhibit  a  predisposition  to  descend 
from  parent  to  child  or  from  grandparent  through  the  unaffected  son 
or  daughter  to  a  grandchild  (in  the  latter  case  it  is  called  atavistic 
hereditary  transmission) . 

The  mode  of  transmission  is  in  all  probability  the  inheritance  of  a 
type  of  tissue,  a  tissue  anatomy  and  physiology  which  permit  the 
more  ready  action  of  the  exciting  causes  of  the  disease.  This  tend- 
ency is  called  a  diathesis — e.g.,  hemorrhagic  diathesis  (haemophilia), 
gouty  diathesis,  or  tuberculous  diathesis. 

Existing  Disease.  The  presence  of  one  disease  may  weaken  the 
resistance  of  a  part  or  the  organism  so  that  another  disease  may  the 
more  readily  become  implanted — e.  g.,  measles  accompanied  by 
pneumonia. 

Previous  Disease.  At  a  period  subsequent  to  disease  the  same 
disease  may  recur  or  another  disease  may  be  implanted — e.  g.,  pneu- 
monia predisposes  a  lung  to  a  recurrence  of  pneumonia  or  tubercu- 
losis may  readily  follow.  Previous  disease  may  confer  immunity 
(which  see). 

Extrinsic  Predisposing  Causes  of  Disease.  Under  this  head  are 
included  all  those  conditions  of  external  origin  which  lessen  the  resist- 
ance of  an  individual  to  the  action  of  exciting  causes.  Excessive  heat 
is  weakening;  cold  and  damp,  by  chilling  the  surface  of  the  body,  cause 
hypersemia  of  internal  parts  and  thus  predispose  to  such  diseases 
as  pneumonia,  rheumatism,  etc.  Fatigue,  unhealthy,  cramping  or 
sedentary  occupations,  continued  loss  of  sleep  from  any  cause,  evil 
habits,  continued  hunger,  etc.,  are  other  examples  of  debilitating 
influences  which  may  be  partly  intrinsic. 

Local  Predisposition. 

Alterations  in  the  normal  physiology  of  a  part  are  apt  to  occur 
through  certain  causes  liable  to  act  upon  it.  Apart  from  this  fact  a 
part  may  be  predisposed,  by  nature  apparently,  to  permit  the  growth 
of  organisms  which  do  not  grow  well  in  other  tissues.  Local  depres- 
sion of  tissue  vitality  predisposes  to  the  growth  of  organisms  in  the 


32  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL. 

tissue.  Mild  injury  producing  hypersemia  of  a  part  or  a  local  anaemia 
(ischsemia)  thus  predispose.  More  severe  injury  also  may  predispose, 
but  the  contrary  effect  has  also  been  observed — i.  e.,  that  severe  injury 
excites  a  phagocytic  reaction  (a  later  stage  of  inflammation)  which 
repels  the  bacterial  invasion. 

The  structure  of  a  part  has  also  been  shown  to  have  an  effect  upon 
the  life  of  organisms  gaining  access  to  its  tissues.  Thus  the  peritoneum 
resists  or  kills  out  pyogenic  cocci  more  successfully  than  other  soft 
parts  or  bones. ^ 

IMMUNITY. 

Immunity  is  the  opposite  of  predisposition  and,  like  it,  can  be  either 
natural  or  acquired.  It  signifies  an  insusceptibility  to  a  disease. 
Natural  immunity  to  a  particular  infectious  disease  can  only  be  deter- 
mined by  repeated  exposures,  and  may  then  fail  at  last  owing  to  some 
systemic  change.  Immunity  may  be  exliibited  toward  only  one  disease. 
In  some  persons  disease  appears  to  be  influenced  by  sex,  as,  for  example, 
males  have  a  general  immunity  from  goitre,  females  from  Addison's 
disease.  Immunity  is  influenced  by  age  in  certain  diseases;  for  ex- 
ample, the  diseases  of  childhood  are  rare  in  the  elderly;  they  do  occur, 
however.  The  degenerative  diseases  of  old  age  are  almost  unknown 
in  childhood.  Race  has  its  influence;  the  negro  is  almost  immune 
to  malaria  and  yellow  fever,  but  particularly  susceptible  to  smallpox 
and  tuberculosis. 

Immunity  may  be  acquired  in  several  ways:  (1)  by  an  individual 
having  passed  through  an  attack  of  a  specific  disease;  (2)  by  inocula- 
tion with  the  attenuated  living  virus  of  the  disease;  (3)  by  inocu- 
lation only  with  the  chemical  products  of  the  virus;  (4)  by  the  intro- 
duction of  the  serum  of  an  animal  inoculated  with  the  chemical 
products  of  a  virus — i.  e.,  by  the  introduction  of  an  antitoxin.  The 
last  process  is  admirably  summarized  by  Green  for  diphtheria  as 
follows : 

1.  "A  pure  culture  of  the  bacillus  diphtherise  (Loeffler)  is  made  in 
a  medium  giving  a  toxin  of  greatest  virulence. 

2.  "The  organisms  are  removed  by  filtration  through  porcelain. 

3.  "The  toxin  thus  obtained  is  injected  into  a  horse  in  small  quan- 
tities two  or  three  times  a  week  until  no  reaction  follows.  This  period 
extends  over  from  one  to  three  months. 

1  Green,  Pathology  and  Morbid  Anatomy. 


IMMUNITY. 


33 


4.  "Some  of  the  blood  is  then  withdrawn  and  the  serum  is  separated, 
steriHzed,  and  stored  for  subsequent  use." 

The  subcutaneous  injection  of  a  small  portion  (about  20  c.c.)  of 
this  substance  will  render  a  person  exposed  to  diphtheria  immune  for 
a  period  of  about  six  weeks.  If  injected  in  the  early  stage  of  an  attack 
it  renders  the  system  more  capable  of  warding  off  the  serious  toxic 
effects  of  the  toxalbumins  produced  by  the  germs. 

In  the  case  of  smallpox  the  Saracens  in  the  sixth  century  introduced 
the  protection  against  the  disease  by  introduction  of  a  minute  quantity 
of  the  virus  from  a  smallpox  pustule  into  the  body  of  a  healthy  person. 
A  mild  attack  ensued,  which  conferred  immunity.  Later,  in  1798, 
Jenner  introduced  inoculation  with  the  virus  from  a  bovine — cowpox 
pustule.  This  practice  of  vaccination  is  still  used  to  confer  immunity 
to  smallpox. 

The  nature  and  action  of  antitoxins  are  unknown.  Ehrlich^  theorizes 
that  the  body  cells  receive  and  neutralize  the  toxin  at  first  presented 
to  them,  and  that  the  cells  under  this  stimulus  form  an  excess  of  the 
neutralizing  substance  (self-formed  antitoxin)  which  floats  in  the 
blood  servmi,  and  therein  combines  with  fresh  portions  of  toxin  absorbed 
from  the  focus  of  infection.  It  is  considered  that  a  special  antitoxin 
is  formed  for  each  form  of  toxin. 

In  the  case  of  serum  therapeutics  as  described  for  diphtheria,  which 
represents  the  principle  involved,  the  antitoxin  is  formed  in  the  bodv 
of  the  horse  instead  of  in  the  human  body.  The  principle  does  not 
seem  to  be  capable  of  application  to  all  varieties-  of  infection.  In 
natural  immunity  there  is  a  healthy  liquor  sanguinis  which  contains 
substances,  probably  of  the  nature  of  nuclein,  which  are  germicidal  for 
bacteria.     These  substances  are  collectively  known  as  "alexins." 

iVccording  to  Emmerich  and  Low  a  third  body,  an  enzyme  formed 
by  the  bacteria,  may  enter  the  blood  and  in  sufficient  concentration 
first  agglutinates  and  then  destroys  the  bacteria  (bacteriolysis).  The 
combinations  of  this  enzyme  with  proteids  are  also  considered  to  have 
bacteriolytic  action.     (See  Chapter  III.) 

1  Yaughan  and  Xovy,  Cellular  Toxins.  ~  % 


CHAPTER  III. 


MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

The  infectious  and  contagious  diseases  have  for  the  most  part  been 
shown  to  be  caused  by  low  forms  of  vegetable  organisms,  while  in  a 
few  diseases  minute  animal  organisms  (protozoa)  are  the  causes. 

The  following  table  shows  the  position  of  the  vegetable  organisms 
in  the  scale  of  vegetable  life  and  gives  the  lowest  forms  of  animal  life: 


f  Phanerogams :  plants  reproducing  by  flowers  and  seeds. 


Vegetable 
kingdom 


Cryptogams, 
reproducing 

by  spore 
formation  or 

division. 


f  Leafy  cryptogams. 


Thallophytes, 

having  no 

distinction 

between  the 

leaf  and  stem. 


1    Lichens. 
1-   Alg£e. 
Fungi    . 


(  Hyphoraycetes 
(mould  fungi). 
I  Blastomycetes 
-!     (bud  fungi). 

Schizomycetes 
(fission  fungi) 


f  Cocci. 
J.  Bacilli. 
(  Spirilla. 


Lowest  form    .  -J 


Protozoa :  single  cells 
without  circulatory  or 
nervous  systems 


Sarcodinea. 
Flagellata. 
Sporozoa. 
Inlusoria. 


Animal 
kingdom 


Higher  forms 


Mycetozoa,  fungi  not  certainly  defined 
as  animal  or  vegetable  forms.' 

Certain  insect  and  worm  forms   are 
pathogenic. 


The  fungi  are  di\4ded  into  (1)  schizomycetes,  or  fission  fungi;  (2) 
hyphomycetes,  or  mould  fungi  (Figs,  6  and  7);   (3)  blastomycetes, 

or  bud  fungi  (or  yeasts)  (Figs.  8  and  9). 
Being  achlorophyllous,  the  fungi  are  un- 
able to  utilize  the  simple  compounds,  such 
as  carbon  dioxide  and  ammonia,  as  foods, 
and  are  therefore  compelled  to  break  down 
the  complex  organic  compounds,  for  which 
purpose  they  are  competent.  All  three 
classes  of  fungi  have  representatives  which 
produce  disease  in  the  human  body,  but  the 
schizomycetes  furnish  by  far  the  greater 
number  of  infectious  disease  causes. 

Of  the  protozoa  four  classes  are  known, 
though  but  few  are  pathogenic  ;  these  classes  are  (1)  the  sarcodinea 
(amoeboid),  which  includes  the  amoeba  dysenteriae  (Fig.  10);  (2)  the 


Trichophj-ton  tonsurans.     Dia- 
grammatic.    (Lehmann.) 


1  The  terms  mycetozoa  and  protozoa  seem  to  be  practically  synonymous  to  pathologists,  who  use 
the  term  protozoa  in  the  sense  of  mycetozoa  as  above  defined. 


MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE.       35 


flagellata,   non-amoeboid   but   motile   by  means   of  flagella  ;    (3)  the 
sporozoa  living  within  the  bodies  of  other  animals,  a  class  which  in- 


FiG.  7. 


Fig.  8. 


a,  saccharomyces ;   6,  cell  with  four 
spores.     (Lehmann.) 


Penicilliiim  with  spores.     (Lehmann.) 
Fig.  9. 


Fig.  10. 


1,  amosba  from  dysenteric  stool, 
with  vacuoles  and  enclosed  red 
cells  ;  2,  amceba  from  straw  in- 
fusion ;  3,  the  same  encysted 
X  600.     (Klinster.) 


Saccharomyces  albicans.     (After  Grawitz,  in  Lehmann.) 


eludes  the  hsemosporidia,  amoeboid  motile  parasites  living  in  the  blood, 
and  of  which  the  hsematozoon  (plasmodium)  malarise  is  an  example 
(Fig.  11);  (4)  the  infusoria. 


36       MICRO-ORGANISMS  AS  EXCITIXG  CAUSES  OF  DISEASE. 

The  schizomycetes  (Greek  schizo,  to  split,  and  mukes,  a  fungus)  are 
minute  single-celled  plants  without  nuclei,  but  possessed  of  a  cell  wall 
and  cell  protoplasm  called  mycoprotein.    They  have  a  size  of  about  one 


/n 


Cycles  of  estivo-autmiinal  parasite.  1.  Very  young  form.  2.  Infection  of  one  cell  with  seven 
young  parasites.  (Drawn  from  a  marrow  smear.)  3.  Triple  infection;  two  parasites  joined 
by  single  chromatin  mass.  4.  Double  infection ;  peculiar  rings  with  two  chromatin  grains  at 
opposite  poles.  5.  Double  infection;  small  ring  adherent  to  cell.  6.  7.  Signet-ring  forms; 
subdivision  of  chromatin.  8,  9.  Later  ring  forms.  Avith  subdivided  chromatin  and  few^ 
pigment  grains.  10-12.  Full-grown  forms  with  finely  subdivided  chromatin  and  gradual  con- 
centration of  pigment.  13.  14.  Stages  of  presegmenting  forms,  with  concentrated  eccentric 
pigment.  1-5.  Double  infection  with  separate  presegmenting  bodies.  16.  Estivo-autumnal 
rosette.  17,  18.  Young  crescent  and  ovoid.  19.  "Pulsating"  crescent.  20-22.  Various  forms 
of  crescents.  23.  Two  bows  about  single  crescent.  21.  Fully  developed  crescent;  two  masses 
of  chromatin ;  achromatic  substance ;  double  •wreaths  of  pigment.  2-5.  Diagrammatic  flagel- 
lating body.     26.  Extracellular  sterile  body.     (Schmaus  and  Ewing.) 

micromillimetre  (1  y-  =  ._,  .5000  inch)  or  less  in  their  smallest  diameter. 
Some  of  them  possess  flagella,  hair-like  processes,  often  very  numerous, 
arising  from  the  protoplasm  rather  than  the  wall,  with  which  they  lash 


MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE.       37 

the  fluid  surrounding  them,  and  by  which  means  they  effect  locomotion 
(Fig.  12).  Other  bacteria  again  are  non-motile.  Entering  the  organic 
compounds,  carbohydrates,  hydrocarbons,  and  nitrogenous  (albumin- 
ous) substances,  they  ferment  or  decompose  them  and  extract  from  them 
substances  necessary  to  their  growth  and  subsequent  reproduction. 


a,  spiral  forms  with  a  flagellum  at  only  one  end;  b,  bacillus  of  tyijhoid  fever  with  flagella 
given  off  from  all  sides ;  c,  large  spirals  from  stagnant  water  with  wisps  of  flagella  at  their 
ends  (spirillum  undula).     (Abbott.) 

The  substance  in  which  they  thus  grow  is  called  the  medium  or  soil. 
The  conditions  under  which  this  is  accomplished  are:  (1)  the  fungi 
must  have  a  proper  vitality;  (2)  their  food  supply  or  soil  must  be  suited 
to  their  growth  and  must  be  moist;  (3)  the  temperature  must  be  suita- 
ble; at  or  near  0°  F.  their  development  ceases,  but  they  are  not  neces- 
sarily killed;  at  160°  F.  maintained  they  usually  die,  but  in  some  cases, 


Typhoid  bacilli — stained  by  Van  Erniengem's  method  to  sho-n'  flagella. 

as  with  the  typhoid  bacilli,  they  may  live  in  the  spore  form  at  even 
212°  F.  unless  maintained  for  some  time.  (4)  Their  waste  products 
must  be  removed  or  they  die  in  them — e.  g.,  in  lactic  fermentation  0.75 
of  1  per  cent,  of  lactic  acid  destroys  the  germs.  Morphologically  the 
schizomycetes  are  grouped  into  several  classes  according  to  form. 


38       MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

1.  ^Micrococci  {mikros,  and  kokkos,  a  berry),  including  all  of  the 
spherical  forms  or  those  having  equal  or  nearly  equal  diameters. 

2.  The  bacilli  {bacillum,  a  rod),  or  rod-like  forms;  one  diameter 
being  greater  than  the  other. 

3.  The  spirillje  (Greek  spira,  a  coil),  or  the  curved  forms. 


Co 


??)•'<?> 


0«^%      0,    ^  ego  °oO    <^ 

C  rf 

C,  staphylococci ;  J),  streptococci ;  c,  diplococci ;  d,  tetrads  :  e,  sarcinje.     (Abbott.) 

x\ll  of  these  groups  may  again  be  subdivided.  The  micrococci  are 
subdivided  according  to  their  modes  of  grouping.  Double  cocci  are 
called  diplococci  {diploos,  double).    If  in  division  the  cocci  agglomerate 

like  a  bunch  of  grapes  they  are  called  staphy- 

^^°'^^"  loeocci  (staphylc,  a  grape).     If  they  arrange 

^^'-^l^^iv^xii t:_  themselves  in  a  chain  they  are  called  strep- 

cZ^j^-~s~C^y''S.~^.j-        tococci  (streptos,  a  chain).     If  they  divide 

'^1.';:: /v'^  -.--r-'v.--  ^       in  two  directions  and  form  a  bunch  of  four 

.'.■r^^^^</'v.v'"-''i'  cocci  thev  are  called  tetrads.    If  in  three 

zobgicea  of  bacilli.   (Abbott.)     directions  they  fomi  sarcinse.     The  bacilli 

are  of  many  and  varied  forms  and  differ 
as  to  their  mode  of  grouping.  During  reproduction  bacteria  may 
excrete  a  material  which  unites  them  into  a  gelatinous  mass  called 
zoogloea. 


^     0  m-o*'*'  O     ° 


a  bed 

a,  bacillus  subtilis  with  spores;  6,  bacillus  anthracis  with  spore.*:  c,  Clostridium  with 

spores;  d,  bacillus  of  tetanus  M'ith  spores. 

The  bacilli  in  the  course  of  reproduction  may  form  long  threads 
showing  as  a  rule  the  traces  of  segmentation.     Under  certain  condi- 


MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE.       39 

tions  the  bacilli  form  glistening  oval  bodies  within  themselves.  The 
body  of  the  bacillus  may  disappear,  leading  the  spore  only.  These 
spores  are  very  resistant  to  devitalizing  agents.  The  bacilli  forming 
spores  are  said  to  be  in  the  resting  stage.  These  spores  under  favor- 
able conditions  again  form  bacilli  like  their  progenitors,  but  do  not 
form  other  spores  without  this  return  to  the  bacillus  form.  A  single 
cell  forms  as  a  rule  but  one  spore.  Under  unfavorable  conditions 
bacteria  may  undergo  degeneration  and  take  on  abnormal  or  involution 
forms,  and  when  the  conditions  are  again  favorable  to  development 
they  may  resume  their  typical  forms.^  A^Hiile  these  form  changes  occur, 
bacteria  are  never  permanently  changed  from  one  form  to  another. 
Those  bacteria  which  have  several  forms  in  their  life  cycle  are  termed 
pleomorphic.  Those  having  but  one  form  are  monomorphic.  Those 
bacteria  which  exist  on  living  tissue  are  known  as  parasitic.  They 
enter  the  body  by  way  of  open  wounds  or  surfaces  deprived  of  epithe- 


FiG.  17. 


a,  spirillum  of  Asiatic  cholera  (comma  bacillus)  ;  6,  involution  forms  of  this  organism 
as  seen  in  old  cultures.     (Abbott.) 

lium  or  may  lodge  at  certain  points  of  the  mucous  surface  of  the  lungs, 
skin  openings,  or  alimentary  canal.  If  not  killed  out  they  multiply 
in  the  natural  juices  of  the  part  on  which  they  locate  and  produce  an 
infective  inflammation.  Toxic  substances  called  toxins  are  generated, 
which  are  absorbed  into  the  system  and  may  act  as  poisons,  produc- 
ing toxaemia.  The  character  of  both  the  inflammation  and  the  poison- 
ing depends  upon  the  particular  bacterium  or  bacteria  present.  The 
bacteria  may  in  certain  cases  be  taken  into  the  blood  and,  coming  to 
rest  at  certain  spots,  the  above-described  process  is  repeated. 

The  bacillus  anthracis  divides  in  the  blood  stream,^  and  other  organ- 
isms, such  as  the  diplococcus  pneumoniae  and  bacillus  influenzae  may 
exist  in  it.  Many  forms  of  organisms  exliibit  a  preference  for  certain 
spots  at  which  they  find  the  conditions  best  suited  to  development 
— e.  cj.,  the  typhoid  bacillus  in  the  glands  of  the  ileum.  Fever's  patches; 
the  anthrax  bacillus  in  the  lungs  of  animals;  the  diphtheria  bacillus 

1  Abbott.  -  Green. 


40       MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

in  the  mucous  surfaces  of  the  pharynx  and  contiguous  parts.  Those 
parasitic  bacteria  which  produce  disease  are  called  pathogenic,  others 
are  non-pathogenic. 

The  mouth  offers  a  suitable  habitat  for  many  bacteria. 

The  bacteria  which  live  on  dead  organic  matter  are  called  sapro- 
phytic (sapros,  rotten,  and  phuton,  a  plant).  They  break  up  the  dead 
animal  and  vegetable  matter  into  simple  compounds  like  carbon 
dioxide,  ammonia,  etc.,  which  are  utilized  by  the  higher  chlorophyllous 
plants.  As  animals  are  dependent  upon  plants  for  existence,  their  vast 
importance  in  the  economy  of  nature  is  evident.  Bacteria  may  often 
pass  from  a  parasitic  existence  to  a  saprophytic  one — a  fact  which  is 
utilized  in  their  study  by  bacteriologists,  who  prepare  artificial  media 
in  which  to  cultivate  them.  These  are  called  cultures,  which  by  trans- 
ference from  one  culture  plate  to  another  of  like  Idnd  are  said  to  be 
passed  through  generations.  ^Mien  by  careful  segregation  one  form 
of  bacterium  is  separated  from  others  present  in  a  mixed  culture  and 
thereafter  cultivated  alone,  it  is  called  a  pure  culture.  Bacteria  may 
pass  from  a  saprophytic  to  the  parasitic  form  of  existence.  Bacteria 
which  have  this  power  of  adaptation  are  called  facultative.  When 
without  this  power  they  are  obligate  bacteria. 

According  to  Pasteur  those  which  require  oxygen  in  order  to  live 
are  called  aerobic.  Those  which  cannot  live  in  its  presence  are  an- 
aerobic.    Those  which  live  either  way  are  facultative. 

FERMENTATION. 

Fermentation  in  the  broadest  acceptation  of  the  term  has  been 
defined  as  the  decomposition  of  substances  possessing  complex  mole- 
cules under  the  influence  of  organized  or  unorganized  ferments.  The 
decompositions  occur  when  organic  substances  are  exposed  to  the 
action  of  bacteria  or  are  subjected  to  the  action  of  certain  substances 
such  as  are  found  in  the  digestive  fluids  secreted  into  the  alimentary 
canal. 

According  to  Woodhead^  the  molecules  of  the  fermented  compound 
are  separated  from  one  another  for  a  brief  period  and  then  allowed  to 
combine  and  form  simple  and  more  stable  compounds.  The  process 
is  accompanied  by  heat  due  to  chemical  changes. 

Ferments,  then,  are  of  two  kinds:  (1)  organized  ferments  or  li\'ing 

^  Bacteria  and  their  Products. 


FERMENTATION.  41 

bacteria  which  multiply  at  the  expense  of  the  substance  which  they  are 
fermenting;  (2)  unorganized  ferments  or  enzymes,  nitrogenous  bodies 
produced  by  living  cells  which  have  the  power  of  producing  chemical 
changes  in  organic  substances.  They  thus  affect  many  times  their 
own  weight  of  the  particular  organic  substance  being  fermented  with- 
out being  themselves  much  affected,  though  eventually  exhausted. 
Typical  examples  are  ptyalin  of  the  saliva,  which  changes  starch  to 
glucose,  and  pepsin  of  the  gastric  juice,  which  changes  albumin  to  pep- 
tone. The  unorganized  ferments  usually  act  by  oxidizing,  deoxidizing, 
or  hydrating  the  substance  modified. 

About  one-third  of  all  pathogenic  bacteria  have  been  shown  to  pos- 
sess such  unorganized  ferments.^  It  is  probable  that  they  produce 
their  effects  on  organic  substances  by  the  aid  of  these  ferments,  which 
serve  them  as  pepsin  serves  man.  It  is  thought  that  in  other  cases 
the  germs  take  up  organic  food,  digest  it,  and  excrete  waste  products 
in  somewhat  the  same  manner  that  the  body  cells  nourish  them- 
selves. As  a  rule  more  than  one  species  of  bacterium  infects  a  ferment- 
able substance.  The  more  active  varieties  predominate  in  the  fer- 
mentation, but  mixed  fermentations  may  proceed.  Some  may  die  out, 
finding  an  unfavorable  soil.  After  a  time  the  predominating  bacteria 
may  die  in  the  waste  products  accumulated  about  them,  leaving 
the  field  clear  for  a  second  or  third  variety.  In  this  way  progressive 
decompositions  may  occur — e.g.,  the  alcoholic  fermentation  may  be 
succeeded  by  the  acetic,  in  which  the  alcohol  is  changed  to  acetic  acid, 
as  in  cider- vinegar  formation.  The  nature  of  the  chemical  changes  pro- 
duced in  a  fermentable  substance  depends  upon  the  chemical  nature  of 
the  latter  and  upon  the  nature  of  the  fungus  causing  the  fermentation. 

Thus  in  an  infusion  of  vegetable  juices  containing  sugar  a  yeast 
fungus  (one  of  the  blastomycetes)  will  produce  carbon  dioxide  gas  and 
alcohol  if  the  oxygen  of  the  air  be  freely  admitted,  while  if  to  a  fresh 
portion  of  the  same  solution  scrapings  from  carious  dentine  be  added 
lactic  acid  will  be  formed  and,  as  a  rule,  no  gas.  Moreover,  the  reac- 
tion will  occur  if  oxygen  be  excluded.^  In  albuminous  compounds  an 
alkaline  reaction  and  entirely  different  substances  will  be  formed  upon 
the  addition  of  carious  dentine. 

The  progressive  decomposition  of  albuminous  matter  into  simple 
compounds  is  effected  by  many  bacteria  through  processes  of  oxida- 
tion, deoxidation,  and  hydration. 

1  Green,  Pathology  and  Morbid  Anatomy.  -  Miller. 


42       MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

Peptones^  are  first  formed,  next  alkaloid-like  bodies  called  ptomaines; 
succeeding  this  such  nitrogenous  bases  as  leucin,  tyrosin,  and  the 
amines  (methyl,  ethyl,  and  propylamine)  are  formed.  Next  fatty  acids 
and  such  acids  as  butyric,  lactic,  and  succinic  acid  appear.  Next 
aromatic  products  such  as  indol,  phenol,  and  cresol  are  formed,  and 
the  final  decomposition  is  represented  in  the  end  products — carbon 
dioxide,  CO^;  hydrogen  sulphide,  H^S;  ammonia,  NH3,  and  water, 
HjO.'  When  bacteria  produce  decomposition  of  living  animal  tissue 
they  effect  this  putrefaction  as  distinctly  noted  in  certain  cases  of  abscess. 

Such  products  of  bacterial  action  either  produced  in  a  living  or  a 
saprophytic  medium  as  are  capable  of  acting  as  poisons  in  the  animal 
organism  are  called  toxins.  Some  animal  parasites  also  produce  them. 
It  is  understood  that  they  differ  according  to  the  fungus  and  the  medium. 
If  the  toxin  be  proteid  in  nature  it  is  termed  a  toxalbumin. 

Some  of  the  ptomaines  are  toxic;  the  greater  number  are  not. 

When  the  toxins  alone  are  absorbed  from  a  focus  of  infection  the 
subject  is  poisoned — a  condition  called  toxaemia,  whether  due  to  a 
toxic  ptomaine,  as  in  the  case  of  Asiatic  cholera,  or  to  a  toxalbumin, 
as  in  the  case  of  diphtheria.  Such  toxaemia  is  commonly  accompanied 
by  more  or  less  fever,  according  to  the  amount  taken  up.  When  the 
organisms  enter  the  circulation  and  multiply  in  the  blood,  or  at  least 
move  about  and  live  in  it  to  be  carried  to  capillaries  in  which  they  can 
rest  and  multiply,  the  condition  is  termed  a  septicaemia.^  In  toxaemia 
and  septicaemia  the  symptoms  depend  upon  the  nature  of  the  organism 
and  their  products.  Bacteria  are  found  everywhere  and  exist  upon 
the  surface  of  the  body,  in  its  external  cavities,  and  in  the  alimentary 
canal.  Here  under  conditions  of  health  there  seem  to  be  conditions 
favoring  certain  forms,  which,  when  implanted,  occupy  the  field  and 
exclude,  except  temporarily,  other  forms  to  which  the  soil  is  not  so 
well  suited.     These  are  known  as  the  "normal  flora." 

With  certain  changes  occurring,  other  forms  may  become  implanted. 
Pathogenic  bacteria  may  exist  in  the  healthy  cavities  and  produce  no 
ill  results.  Again,  the  soil  may  favor  and  disease  begins.  Certain  bac- 
teria have  been  found  constantly  present  in  relation  with  certain  dis- 
eases— e.  g.,  the  spirillum  of  Asiatic  cholera  with  that  disease.  These 
are  specific  bacteria.  Taken  from  individuals  with  the  disease,  they 
produce  it  in  susceptible  animals  inoculated  with  them  if  circum- 
stances favor  their  growth. 

'-  Ziegler's  General  Pathology. 
2  Abbott. 


FERMENT  A  TION. 


43 


Bacteria  spread  in  the  tissue  along  the  lines  of  least  resistance. 
They  may  follow  the  cellular  tissue  or  enter  the  lymphatics,  or  pass 
at  once  into  the  veins  and  be  carried  into  the  circulation.  They  may 
be  strictly  localized  at  the  point  of  infection. 


Fig.  19. 


Staphylococcus   pyogenes   aureus.      From   a 
culture.     X  1000.     (Green.) 


Streptococcus  pyogenes.     From  pus  found  in 
a  pysemic  abscess.     X  1000.     (Green.) 


R 


Fig.  20. 


~^^ 


IWe 


.■   %^ 


^W      it 


t 
^ 


Mouse's  lung;  vessels  plugged  with  bacilli  anthracis.     a,  alveolus;   (',  vein  full  of  bacilli; 
c,  capillaries  also  full ;  hr,  bronchus.     X  400.     (Horsley.) 

Thus  there  may  be  a  localized  inflammation — e.  g.,  in  simple  abscess 
due  to  the  staphylococcus  pyogenes  aureus;  a  diffuse  inflammation, 
as  in  case  of  infection  by  the  streptococcus  pyogenes ;  or  a  metastatic 
inflammation,  as  in  pyaemia,  in  which  the  germs  (usually  S.  pyogenes) 
gain  access  to  the  blood  from  a  local  focus  of  infection  and  are  carried 
to  distant  parts,  in  which  they  cause  inflammation.     To  produce  effect 


44       MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

germs  in  the  blood  must  come  to  rest  at  some  point,  which  may  occur 
in  the  capillaries  owing  to  their  injury,  in  thrombi  or  emboli,  or  in 
case  of  entrance  of  bacteria  into  a  leukocyte  they  may  migrate  into 
the  connective  tissue  (Fig.  20). 

It  has  been  shown  that  pyogenic  germs  may  exist  in  the  blood  with- 
out local  effects,  while  again  a  local  injury  may  cause  the  arrest  of  the 
germs  and  a  secondary  local  inflammation  or  abscess  be  set  up.  This 
is  due  to  simple  arrest  or  to  extravasation  of  blood,  which  permits  the 
germs  to  pass  from  the  vessels  into  the  connective  tissue. 

General  or  local  depression  of  tissue  vitality  acts  as  a  predisponent 
to  local  infection. 

The  infections  themselves  are  classified  as  primary,  secondary,  and 
mixed. 

The  primary  is  the  original  infection,  say,  e.g.,  bacillus  tubercu- 
losis. The  secondary  is  that  implanted  when  the  original  disease  is 
well  under  way — e.g.,  S.  pyogenes  aureus  upon  tuberculosis;  a  third 
or  tertiary  infection  is  possible.^ 

The  original  infection  may  be  by  mixed  germs,  more  than  one  of 
which  may  multiply.  Thus  the  S.  pyogenes  aureus  and  diplococcus 
pneumonise  may  both  be  found  in  an  abscess.    This  is  mixed  infection. 

BACTERIA  OF  THE  MOUTH. 

In  even  the  best  cared  for  mouths  bacteria  are  numerous  and  find 
the  conditions  suited  to  their  growth.  In  unclean  mouths  containing 
food  debris,  dead  epithelium,  etc.,  their  life  conditions  are  much  more 
favorable.  According  to  Miller^  there  are  a  number  of  bacteria  which 
almost  invariably  occur  in  every  mouth.    These  are: 

1.  Leptothrix  innominata. 

2.  Bacillus  buccalis  maximus. 

3.  Leptothrix  buccalis  maxima. 

4.  Jodococcus  vaginatus. 

5.  Spirillum  sputigenum. 

6.  Spirochsete  dentium  (denticola). 
To  this  list  Goadby''  has  added: 

Leptothrix  racemosa  of  Vicentini,  further  described  by  Williams.* 
Streptococcus  brevis  of  Lingelsheim,  and  Cladothrix  buccalis  (pro- 
visionally added). 

1  Park,  Surgery  by  American  Authors.  -  Micro-organisms  of  the  Human  INIouth. 

3  Mycology  of  the  Mouth,  1903.  *  Dental  Cosmos,  1899.    See  Dental  Caries. 


BACTERIA  OF  THE  MOUTH. 


45 


With  the  exception  of  S.  brevis  and  perhaps  Cladothrix  and  B.  buc- 
caHs  maximus  these  are  uncultivable  on  laboratory  media,  are  strictly 
obligate  parasites.  Of  the  last-named  organism  Goadby  obtained 
biological  characteristics  of  the  pure  culture,  but  did  not  establish  its 
disease-producing  power,  if  any. 

Certain  pathogenic  organisms  have  been  shown  to  be  present  in 
the  mouths  of  healthy  persons,  such  as  bacteriological  investigators; 
those  nursing  infectious  diseases,  such 
as  diphtheria,  scarlet  fever,  etc.,  and 
even  in  the  mouths  of  healthy  indi- 
viduals apparently  not  exposed  to  any 
infection.     In  about  10  per  cent,  of 
all  individuals  examined  at  random 
Netter  found  staphylococcus  pyogenes 
aureus  (golden  pus) .     Staphylococcus 
pyogenes  albus  was  also  found.    The 
pneumococcus  or  diplococcus   pneu- 
moniae was  found  in  the   mouths  of 
about    15  per  cent,  of   healthy  indi- 
viduals.    This    organism    has    been 
found  by  Kirke  to  be  apparently  caus- 
ative of  pericemental  abscess,  and  has 
been  reported  by  Schreier^  as  found  in 
75  per  cent,  of  cases  of  apical  abscess 
examined.    It  has  also  been  related  with  cases  of  osteomyelitis.     The 
bacillus  diphtheriae  of  Loeffier  has  been  found  in  about  10  per  cent, 
of  mouths  examined  at  random,  and  33  per  cent,  of  600  children  in  a 
school  examined  during  an  epidemic  of  diphtheria  were  found  to  have 
the  bacillus  present  in  the  mouth,  while  but  about  2  per  cent,  developed 
the  disease.^    This  latter  fact  shows  the  absolute  necessity  for  a  pre- 
disposition as  well  as  an  exciting  cause 

The  bacillus  tuberculosis  exists  in  the  mouths  of  many  suffering 
from  pulmonary  tuberculosis,  and  exists  also  at  times  in  the  mouths 
of  the  healthy.  Primary  tubercular  osteitis  has  been  observed.  The 
saccharomyces  albicans  may  be  present  and  at  times  produce  thrush 
(Fig.  9). 

The  bacillus  typhosus  (typhoid)  has  been  found  in  the  healthy 
mouth,  and  at  times  has  oral  pathogenicity.  Many  other  organisms 
have  been  isolated  from  the  human  mouth.    Some  of  these  have  specific 


Diplococci  pneumoiiise  entangled  in 
the  meshes  of  the  fibrinous  exudation. 
From  a  section  of  lung  in  the  "  red  hepa- 
tization" stage  of  acute  pneumonia.  In 
the  upper  part  of  the  field  is  a  cell  con- 
taining several  cocci — possibly  a  phago- 
cyte.    X  1000.     (Green.) 


1  Dental  Cosmos,  1893. 


Goadby. 


46        MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

character,  of  others  Uttle  is  known.  Some  of  the  bacteria  of  the  mouth 
possess  the  power,  under  certain  conditions,  of  felting  themselves  in  a 
gelatinous  mass  or  film  upon  the  surfaces  of  the  teeth.    Here  if  prop- 


Bacilliis  diphtherise.    A.  Its  morphology  on  glycerin-agar-agav.    B.  Its  morphology  on  Loeffler's 
blood  serum.     C.  Its  morphology  on  acid  blood-serum  mixture.     (Abbott.) 


Fig.  23. 


\ 


/ 


^/ 


erly  supplied  with  carbohydrate  food  some  of  them  produce  lactic  acid 
and  decalcify  the  teeth.  Some  have  a  later  putrefactive  action  upon 
the  organic  matrix  of  the  dentine.  Goadby^  gives  an  interesting  classi- 
fication of  bacteria  found  in  dental  caries 
(which  see).  Some  bacteria  not  yet  isolated 
are  the  probable  causes  of  pyorrhoea  alveolaris. 
The  bacteria  in  the  mouth  probably  are 
taken  into  the  food  and  swallowed  in  great 
numbers.  Many  are  doubtless  killed  by  the 
gastric  juice,  which  is  a  weak  germicide;  not- 
withstanding, some  pyogenic  cocci  and  some  of 
the  blastomycetes  may  develop  in  the  stomach 
and  produce  disease.  Many  also  may  enter 
the  intestines  and  either  excite  disease  of  spe- 
cific character  or  produce  abnormal  intestinal  fermentations  the  toxins 
of  which  may  be  absorbed.  They  may  remain  localized  in  the  mouth 
and  produce  oral  disease,  dental  caries,  or  pericemental  diseases,  etc. 


\ 


N 


> 


\ 


Bacillus  tuberculosis. 
X  1000.    (Green.) 


^   Mycology  of  the  ^Alouth 


THE  RESISTANCE  OF  THE  TISSUES  TO  INFECTION.  47 

The  relation  of  an  unclean  mouth  to  effects  upon  the  mouth  and 
alimentary  canal  and  air  passages  is,  therefore,  a  direct  one  of  an 
importance  that  renders  exact  studies  in  this  direction  of  extreme 
value.  Unfortunately  the  problem  is  but  partially  worked  out.  (See 
Pyorrhoea  Alveolaris.) 

THE   RESISTANCE  OF  THE  TISSUES  TO   INFECTION. 

The  resistance  of  the  tissues  to  bacteria  is  to  be  considered  from 
two  main  standpoints: 

1.  The  prevention  of  the  entrance  of  bacteria  into  the  tissues. 

2.  The  destruction  of  the  bacteria  after  entrance  into  the  tissues. 
(1)  The  prevention  of  entrance.    It  has  been  shown  that  pathogenic 

bacteria  may  enter  the  mouth,  alimentary  canal,  lungs,  etc.,  but  few 
develop. 

The  skin  acts  as  a  mechanical  barrier,  though  its  openings  may  at 
times  harbor  bacteria. 

Fig.  24. 


1,  a  spore  ^vliicli  has  penetrated  the  intestinal  -^val)  and  entered  the  abdominal  cavity,  ^vhere 
four  leukocj-tes  have  surrounded  its  end :  in,  the  muscular  layer  of  the  intestine ;  e,  epithelial 
layer ;  s,  the  serous  layer.  2,  a  spore  surrounded  by  leukocytes  from  the  abdominal  cavity  of 
a  Daphne.     (Metchnikoil. ) 

The  mucous  membrane  secretes  mucus,  which  envelops  bacteria 
and  with  it  they  are  carried  away.  The  healthy  mucus  also  has  appar- 
ently a  devitalizing  power  tor  some  bacteria,  not  for  others.  The  acid 
gastric  juice  kills  many  and  probably  the  intestinal  juices  also  inhibit 
in  large  degree  the  action  of  such  as  have  entered  the  alimentary  canal. 
In  all  cases  the  agitation  of  the  fluids  of  a  part  seems  to  act  mechanic- 
ally to  prevent  localization  of  bacteria. 

(2)  The  prevention  of  development  in  the  tissues.  Within  the 
healthy  tissues  bacteria  find  several  elements  opposing  their  devel- 
opment. 

It  seems  the  concensus  of  opinion  of  pathologists  that  the  blood 
serum  contains  a  germicidal  substance  or  substances  probably  of  the 
nature  of  a  nuclein  and  called  by  Buchner  "alexin." 

This  belief  is  mainly  based  upon  the  demonstrations  of  Nuttall  that 


48       MICRO-ORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 

filtered  blood  serum  possesses  the  power  of  producing  the  degenera- 
tion of  bacteria.  Buchner  found  that  heating  to  55°  C.  destroyed 
this  property,  a  fact  pointing  to  the  albuminous  nature  of  the  alexins. 
After  reviewing  all  the  evidence  Vaughan  and  Novy^  conclude:  "(1) 
the  exact  nature  of  the  germicidal  constituents  of  the  blood  or  alexins 
is  not  known ;  (2)  the  alexins  have  their  origin  in  the  white  blood  cor- 
puscles; (3)  disintegration  of  the 
white  blood  corpuscles  liberates 
alexins;  (4)  it  is  probably  true 
that  alexins  are  also  secreted  by 
living  leukocytes." 

Metschnikoff,  in  1884.  demon- 
strated that  the  leukocytes  take 
up  bacteria  within  themselves 
and  claimed  that  they  thus  de- 
stroy them.  This  process  he 
termed  phagocytosis  (phago,  I 
eat;  cytos,  a  bud).  It  is  now 
considered  that  this  property, 
which  is  also  possessed  by  the 
endothelial  cells  of  the  blood- 
vessels and  by  the  fibroblasts,  is 
but  evidence  of  the  nutritive 
function  of  simple  cells  occur- 
ring after  the  bacteria  have  been 
partially  degenerated  by  the  se- 
rum (Fig,  25).  If  the  conclu- 
sions of  Vaughan  and  Nov)'  be  correct,  that  the  alexins  are  furnished 
by  the  leukocytes,  it  would  seem  quite  possible  that  the  destruction 
of  some  of  the  bacteria  may  be  produced  within  the  leukocytes. 
Researches  of  Leber,  Buchner,  and  others  have  shown  that  leukocytes 
may  be  attracted  by  certain  bacterial  products  even  in  high  dilution 
and  by  other  chemical  substances,  such  as  mercury  and  copper  salts. 
This  is  called  positive  chemotaxis.  Other  substances,  such  as  methyl- 
amin,  leucin,  tyrosin,  and  urea,  exliibit  a  repulsion — negative  chemo- 
taxis. 

If  the  combined  local  forces  be  incompetent  to  kill  out  the  infect- 
ing organisms  the  local  infection  spreads  until  limited  or  the  patient 


Active  phagocytosis.  Endothelial  cells  en- 
closing the  bacilli  of  swine  septieseniia,  from  an 
hepatic  vein  of  a  pigeon:  a.  endothelial  cells; 
6,  leukocytes.     (MetschnikofE.) 


1  Cellular  Toxins,  1902. 


EXTERNAL  ANTIBACTERIAL  INFLUENCES.  49 

dies,  or  a  metastasis  may  occur,  in  which  case  the  process  is  practically 
repeated  in  another  locality. 

The  absorbed  toxins  may  produce  a  toxsemia  in  either  case;  a  reac- 
tion takes  place  upon  the  part  of  the  body  cells  generally  and  new 
substances  enter  the  blood,  which  are  not  necessarily  fatal  to  the  organ- 
isms themselves,  but  act  as  antidotes  to  their  toxins,  which  they  neu- 
tralize^— i.  e.,  they  are  self-formed  antitoxins.  (See  Immunity.)  A  third 
body  may  exist  in  the  blood  after  infection,  consisting  of  an  enzyme 
produced  by  the  bacteria,  and  which  after  reaching  a  certain  degree 
of  concentration  may  first  agglutinate  the  bacteria  in  masses  (agglu- 
tination) and  later  dissolve  them  (bacteriolysis).  This  action  may 
occur  either  in  old  cultures  out  of  the  body  or  in  the  blood,  etc.,  mthin 
the  body.^  The  general  name  of  nucleases  has  been  proposed  for 
these  ferments. 

Combining  with  certain  normal  albuminous  bodies  in  the  blood 
they  produce  combinations  known  as  immune  proteids,  which  retain 
the  original  bacteriolytic  properties  of  the  enzymes  and  in  some  cases 
have  antitoxic  properties  as  well. 

Emmerich  and  Low,  who  are  responsible  for  the  above  formula- 
tions, claim  that  experimentally  the  enzyme  of  bacillus  pyocyaneus 
(pyocyanase)  and  its  immune  proteids  (pyocyanase-immune  proteids) 
are  bacteriolytic  for  B.  pyocyaneus  and  the  bacteria  of  anthrax,  typhoid, 
diphtheria,  pest,  and  Asiatic  cholera.'^ 

The  theory  as  demonstrated  runs  somewhat  counter  to  that  of 
Ehrlich's  theory  of  antitoxin  formation  (see  p.  33)  and  both  are 
necessarily  suh  judice. 

EXTERNAL  ANTIBACTERIAL   INFLUENCES. 

Many  chemical  substances  and  physical  forces  prevent  the  growth 
and  reproduction  of  bacteria  without  necessarily  killing  them;  these 
are  called  antiseptics;  a  weak  solution  of  boric  acid  is  an  example, 
agitation  is  another,  dryness  another.  Other  substances  or  forces 
kill  the  bacteria  after  an  exposure  to  their  influence  for  a  sufficient 
length  of  time;  these  are  germicides — e.g.,  a  1:  1000  solution  of  mer- 
curic chloride  in  water,  boiling  water,  or  streaming  steam;  light  for 
some  bacteria.  Other  substances  destroy  both  the  bacteria  and  their 
products;  these  are  disinfectants — e.g.,  sodium  dioxide  or  other  sub- 
stances liberating  nascent  oxygen. 

1  Ehrlich.  2  Vaughan  and  Novy.  *  Ibid. 

4 


CHAPTER   IV. 

DISTURBAXCES  OF   NUTRITIOX. 

Disorders  of  nutrition  are  of  three  classes:  (1)  due  to  an  excess  of 
nutritive  material;  (2)  due  to  a  deficiency  of  nutritive  material;  (3) 
due  to  the  presence  in  the  blood  of  material  which,  instead  of  serv- 
ing the  purpose  of  metabolism,  disturb  it. 

EXCESS  OF  NUTRITION.     HYPERNUTRITION. 

An  excess  of  nutrition  may  be  either  general  or  local.  In  either 
case  it  is  associated  with  an  overfulness  of  the  bloodvessels  (hyper- 
£emia).  If  the  individual  possess  this  general  overfulness  of  vessels 
he  is  said  to  be  plethoric.  Sthenic  plethora  is  such  an  overfulness 
associated  with  activity  of  the  circulation  and  a  consequent  increase 
of  the  vital  processes  due  to  plentiful  cell  nutrition,  and  with  an  active 
repair  of  even  excessive  Avaste  of  cell  protoplasm. 

In  asthenic  plethora,  on  the  contrary,  the  vessels  are  overful,  but  the 
circulation  is  sluggish;  waste  products  are  probably  accumulated  in 
the  blood  and  the  vital  processes  are  sluggish  in  consequence.  In- 
stead of  the  rich  color  and  active  movements  associated  with  sthenic 
plethora,  the  asthenic  have  a  purplish  appearance  and  the  movements 
are  more  labored. 

Local  Hypernutrition.  An  increased  stimulation  of  the  nerves  of 
a  part  invites  more  blood  to  it,  which  within  certain  limits  increases 
the  nutrition  to  the  cells  of  the  part.  This  results  in  increased  irri- 
tabilitv,  contractility,  and  general  functional  activity  of  the  function- 
ating cells.  If  this  be  maintained  the  cells  grow  or  multiply  or  both, 
and  the  part  is  enlarged  and  capable  of  an  increased  amount  of  work. 

Stimulation  beyond  this  point  causes  irritation  or  overstimulation 
of  cells  and  the  vital  processes  become  fretful,  incomplete  chemical 
changes  occur  in  the  cells,  and  the  functional  activity  is  disordered. 
The  cells  are  wearied  and  if  the  overstimulation  be  continued  par- 
alysis from  overwork  results. 

Hypertrophy.  Though  strictly  meaning  an  excess  of  nutrition, 
this  term  signifies  an  increase  in  size  of  a  part  due  to  an  increase  of 


EXCESS  OF  XUTPJTIOX.    HYPERXUTRITIOX.  51 

nutrition.  The  new-growth  must  be  practically  normal  in  structure. 
As  a  rule  both  the  size  (simple  hypertrophy)  and  number  of  the  cells 
(numerical  hypertrophy  or  hyperplasia)  are  increased.  The  calibre  of 
the  bloodvessels  is  increased  to  comply  with  the  stimulus  to  their  con- 
trolling nerves — the  vasomotors.  Hypertrophy  is  frequently  exhibited 
in  tissues  subjected  to  an  unusual  amount  of  work  short  of  marked 
fatigue.  An  increase  in  its  function  occurs;  its  capacity  for  work 
becomes  greater,  and  if  the  strong  stimulus  (mild  irritation)  implied 
be  continued  the  cells  increase  in  size  and  it  may  be  in  number,  all 
three  phases  of  the  expenditure  of  an  increase  of  vital  energy  being 
represented — functional,  nutritive,  and  reproductive.  If  the  heart 
be  subjected  to  an  increase  in  the  strain  ordinarily  brought  upon  it 
an  increase  in  the  volume  of  the  muscular  fibres  follows,  causing  hyper- 
trophy of  the  walls.  The  same  is  true  of  the  muscles  of  the  gravid  uterus, 


Dog's  hail-  encapsulated  in  subcutaneous  tissue :  a,  hair ;  b,  fibrous  tissue ;  C,  proliferating- 
granulation  tissue ;  d,  giant  cells.  Preparation  hardened  in  alcohol,  stained  with  Bismark 
brown,  and  mounted  in  Canada  balsam.     X  66.     (Ziegler.) 

in  which  the  cells  increase  to  many  times  their  normal  length.  When 
one  organ,  as  a  kidney,  takes  up  alone  the  work  usually  performed 
by  two  it  increases  in  size  (hypertrophies).  This  is  called  compen- 
satory hypertrophy.  It  may  occur  in  an  organ  which  endeavors  to 
supply  the  deficient  function  in  another  organ  of  different  sort.  Hyper- 
trophy also  occurs  in  many  inflammatory  conditions,  and  is  due  to 
the  area  of  hypersemia  surrounding  every  focus  of  inflammation. 
Thus  the  epithelium  about  the  edges  of  an  ulcer  may  thicken  or  new 
bone  may  be  formed  about  an  area  of  inflamed  bone  tissue  or  perios- 
teum. The  bone  tissue  may  become  more  compact,  a  condition  termed 
sclerosis  of  bone,  as  it  results  in  the  formation  of  formed  (intercellular) 
tissue  at  the  expense  of  the  cellular  elements. 

The  removal  of  an  accustomed  resistance  often  produces  an  irrita- 
tion  resulting  in  mild   hypersemia   and  thickening  or  hypertrophy 


52  DISTURBANCES  OF  NUTRITION. 

results  —  ^- 0-,  non-occlusion  of  teeth  frequently  produces  hyper- 
ceraentosis. 

A  form  of  cellular  hypertrophy  appears  to  occur  in  certain  leuko- 
cytes, resulting  in  the  formation  of  a  multinucleated  cell  or  "giant 
cell." 

Under  irritation  the  nucleus  subdivides,  but  the  cell  body  fails  of 
division,  and  instead  of  complete  reproduction  a  large  cell  with  many 
nuclei  is  formed  (Fig.  26).  These  cells  appear  where  tissue  is  to  be  re- 
moved, as  in  the  case  of  aseptic  foreign  bodies  or  the  roots  of  deciduous 
or  even  of  permanent  teeth.  (See  Resorption  of  Temporary  Teeth.) 
An  hypertrophy  or  excessive  development  may  occur  during  intra- 
uterine life  and  is  spoken  of  as  congenital  hypertrophy.  A  low  grade 
of  inflammation  may  lead  to  a  numerical  hypertrophy,  as  in  the  case 
of  hypertrophy  of  the  dental  pulp  (which  see). 

Cyst  and  Tumor  Formation.  A  cyst  is  an  enlargement  containing 
a  cavity  which  in  turn  contains  liquid,  gelatinous,  or  pultaceous  mate- 
rial about  which  is  a  capsule  condensed  from  the  surrounding  struc- 
tures. The  accumulation  of  the  fluid  or  semifluid  contents  pro- 
duces the  enlargement  of  the  part  even  if  bony  (Fig.  27). 

They  differ  from  tumors  in  being  strictly  localized,  though  they 
may  be  large,  and  in  their  generally  benign  character,  though  tumors 
may  at  times  have  a  cystic  character. 

Cysts  may  be  formed  by  the  retention,  secretion,  or  extravasation 
of  fluid  in  several  ways:  (1)  By  the  retention  of  normal  secretion  of 
a  gland  owing  to  the  obstruction  of  its  duct— e.  g.,  ranula.  These 
are  called  retention  cysts.  (2)  By  abnormal  secretion  into  ductless 
cavities — e.  g.,  bursse  (exudation  cysts).  (3)  By  the  extravasation 
of  blood  into  a  ductless  cavity  (extravasation  cyst).  (4)  Independ- 
ently in  tissue  as  a  result  of  mucoid  or  fatty  changes  or  liquefaction 
necrosis,  the  surrounding  tissue  becoming  condensed  into  a  capsule. 
(5)  Independently  as  a  collection  of  fluid  in  connective-tissue  spaces, 
which  enlarge  and  fill.  The  surrounding  tissue  condenses  into  a  cyst 
wall.  (6)  Independently  as  a  result  of  chronic  irritation  by  foreign 
bodies,  extravasated  blood,  or  parasites,  as  in  dentigerous  cysts^  (Fig. 
27).  Cysts  may  have  but  one  cavity  (simple  cysts)  or  have  numerous 
intercommunicating  ca^dties  known  as  loculi  (compound  or  multi- 
locular  cysts).  Forming  mthin  bony  walls,  these  may  be  largely 
distended  and  the  walls  are  usually  thin.  Dentigerous  and  other 
cysts  are  usually  lined  by  epithelium  peculiar  to  the  part. 

1  Green. 


EXCESS  OF  NUTRITION.     HYPERNUTRITION. 


53 


Dermoid  cysts  are  cystic  tumors  of  widely  varjdng  sizes  found  in 
various  parts,  such  as  the  ovary,  neck,  base  of  brain,  orbit,  etc.  They 
contain  fatty  debris,  and  are  Uned  with  epithehum,  outside  of  which  is  a 
corium  with  its  papillae,  and  outside  of  this  subcutaneous  adipose  tissue. 
The  whole  is  enclosed  in  a  fibrous  capsule  of  connective  tissue.  The 
epithelial  lining  may  contain  and  develop  the  characteristically  der- 
moid structures,  hair,  teeth,  sebaceous  and  sweat  glands^  (Fig.  28). 

Dermoid  cysts  are  classed  with  the  teratomata  or  monsters  considered 
as  partially  developed  fetal  structures  attached  to  the  surviving  foetus. 


Fig.  27. 


Cyst  of  the  lower  jaw,  having  its  origin  about  an  undeveloped  tooth      (Garretson.) 

A  tumor  is  a  new-growth  conforming  to  a  degree  to  the  normal  his- 
tology of  a  part,  but  having  no  physiological  function  and  no  typical 
limit  of  growth.  They  are  classed  as  benign  or  malignant  accordingly 
as  they  are  strictly  localized  and  comparatively  harmless  or  tend  to  sap 
vitality  and  to  spread  dangerously  or  to  be  transferred  to  other  locali- 
ties (metastasis). 

The  growth  of  a  tumor  is  attended  by  a  sapping  of  the  vitality  of  a 
sufferer^ — the  degree  of  the  debility  produced  being  apparently  in 
direct  ratio  to  the  size  and  the  rapidity  of  the  growth.  Besides  the  size 
and  the  rapidity  of  development  of  individual  tumors,  another  -element 
determines  their  malignancy,  their  position,  and,  furthermore,  their 
occurrence  in  other  parts,  resulting  in  multiple  tumor  formation.     A 


'  Zieglei'. 


54 


DISTURBANCES  OF  NUTRITJOX 


tumor  victim  acquires  a  peculiar  appearance — a  cachexia,  whose  inten- 
sity and  rapidity  of  advance  are  directly  dependent  upon  the  degree  of 
mahgnancy. 

Tumors  introduce  no  new  form  of  tissue  element;  they  are  repro- 
ductions of  the  cells  of  the  tissues  of  the  body.  They  may  have  the 
same  cell  formation  as  the  tissue  from  which  they  spring,  and  are  then 
called  homologous  tumors;  or  they  may  have  a  different  histological 
structure  from  the  tissue  in  which  thev  are  found,  being  then  called 


Portion  of  a  ^vall  of  an  ovai'ian  dermoid  cyst:  a,  wall  of  the  cyst:  b,  projecting  portion  made 
up  of  fatty  and  cutaneous  tissue ;  c,  hairs;  d,  teeth.     (Ziegler.) 

heterologous  tumors.  For  example,  a  bony  tumor  growing  from  bone 
W' ould  be  homologous ;  a  cartilaginous  tumor  growing  from  gland  tissue 
would  be  heterologous. 

Causes.  The  causes  of  tumor  formation  are  unknown;  it  has  been 
believed  that  their  growth  is  due  to  parasites,  especially  the  protozoa; 
this,  however,  has  not  been  proved.  A  certain  proportion  of  tumor 
formations,  7  to  14  per  cent.,^  appear  to  be  caused  by  traumatic  injury; 


1  Ziejjfler. 


EXCESS  OF  NUTRITION.     HYPERNUTRITION.  55 

as,  for  example,  in  cases  of  mammary  tumor,  a  history  of  a  blow  or  fall 
may  be  at  times  obtained. 

Long-continued,  sluggish  inflammation  appears  to  be  causative  of 
tumor  formation  in  an  unknown  percentage  of  cases.  A  chronic  irrita- 
tion of  certain  portions  of  the  body,  such  as  the  junction  between  the 
mucous  and  skin  surfaces  of  the  lip,  the  sides  of  the  tongue,  etc.,  is  a 
frequent  antecedent  to  their  formation.  Ziegler  gives  a  reasonable 
explanation  of  the  origin  of  certain  epithelial  tumors  in  organs  which 
are  undergoing  atrophy;  for  example,  in  advanced  age  the  connective 
tissue  of  the  body  is  undergoing  atrophy  and  there  is  relaxation  of  its 
strata;  the  epithelium  of  the  surface  (or  of  glands),  still  possessed  of  its 
power  of  reproduction,  proliferates  and  invades  the  connective  tissue, 
producing  cancer. 

Tumor  formation  consists  in  the  reproduction  of  the  cells  of  one  or 
more  tissues,  and  in  the  growth  thus  formed  bloodvessels  are  developed. 
Tumors  do  not  contain  nerves.  Their  blood  supply,  however,  is  gen- 
erous, so  that  for  long  periods  a  superabundance  of  nutritive  material 
is  carried  to  them;  but  after  a  variable  period,  depending  upon  the 
type  of  growth,  the  nutritive  supply  becomes  disordered  and  degenera- 
tions occur. 

About  the  more  slowly  developing  tumors  a  condensation  of  con- 
nective tissue  occurs  in  many  cases,  forming  a  distinct  limiting  wall 
or  capsule  from  which  the  tumor  may  be  enucleated.   , 

The  two  great  classes  of  tumors,  those  of  mesoblastic  and  those  of 
epiblastic  and  hypoblastic  origin,  may  be  subdivided  into  orders  accord- 
ing to  their  histological  peculiarities. 

Class  One.^ 

tumors  of  mesoblastic  tissues. 

Order  One. 
Tumors  of  mature  connective  tissue: 
Bony  tumors,  or  Osteoma. 
Cartilaginous  tumors,  or  Chondroma. 
Fibrous  tumors,  or  Fibroma. 
Fatty  tumors,  or  Lipoma. 
Mucous  tumors,  or  Myxoma. 
Lymphoid-tissue  tumors,  or  Lymphoma. 

1  Modified  from  Green's  Pathology,  p.  148. 


66  DISTURBANCES  OF  NUTRITION. 

Order  Tico. 
Tumors  of  the  embryonic  connective  tissues: 
The  fleshy  tumors,  or  Sarcoma. 

Order  Three. 
Tumors  of  the  higher  tissues: 

Tumors  of  muscle,  or  Mvoma. 

Tumors  of  nerves,  or  Neuroma. 

Tumors  of  bloodvessels,  or  Angioma. 

Tumors  of  Imiphatic  vessels,  or  L^Tnphangioma. 

Class  Two. 

tuiviors  of  epiblastic  axd  hypoblastic  tissues. 

Papilla  of  skin  and  of  mucous  membrane,  or  Papilloma. 

rj^  £    1     J  1      X-  ^  Adenoma. 

i  umors  or  glandular  tissue  -,  ^ 

i  Carcinoma. 

The  tumors  of  epiblastic  and  hypoblastic  type  are  sometimes  called 
Epitheliomata,  for  epithelial  tissue  is  their  characteristic  histological 
structure. 

Malignant  tumors  are  found  in  both  of  the  great  classes,  mesoblastic 
and  epiblastic  and  hypoblastic.  Carcinoma  represents  the  type  of 
malignancy  in  the  epithelial  tumors.  The  sarcomata  are  the  malignant 
tumors  of  the  connective-tissue  type. 

Tumors  are  rarely  composed  of  but  one  type  of  tissue;  several  types 
may  be  present,  the  tumor  receiving  its  name  from  the  tissue  predomi- 
nating. "\Mien  the  distinguishing  feature  of  a  tumor  is  two  predominat- 
ing tissues,  the  tumor  is  given  a  compound  name;  as,  for  example, 
when,  in  a  sarcomatous  gro\^i:h,  numerous  large  multinucleated  cells 
characteristic  of  bone-marrow  are  found,  it  is  called  a  myeloid  sar- 
comatous tumor.  ^Mien  fibrous  and  sarcomatous  tissues  are  distin- 
guishing features  the  tumor  is  called  a  fibrosarcoma. 

Since  the  malignancy  of  a  tumor  is  due  primarily  to  the  size  and  the 
rapidity  of  its  growth,  it  is  clear  why  sarcomata  are  more  malignant 
than  fibromata,  and  why  some  forms  of  sarcoma  are  more  malignant 
than  others.    To  illustrate: 

Begin  observation  at  the  indifferent  stage  of  connective-tissue  devel- 
opment, when  connective-tissue  cells  have  first  di^dded,  reproduced; 
the  tissue  produced,  seen  in  granulation  tissue  and  in  the  embryo,  is  at 


EXCESS  OF  NUTRITION.    HYPERNUTPdTION. 


57 


the  indifferent  stage,  as  seen  in  section  of  the  embryonic  jaw 
(Fig.  29). 

Mesoblastic  cells  at  this  early  period  are  in  an  indifferent  stage;  some 
of  the  cells  shown  in  the  figure  will  form  bloodvessels,  others  ^\dll 
become  bone  corpuscles,  others 
will  form  fibrous  and  others 
muscular  tissue.  This  struc- 
ture has  its  analogue  among 
tumors  in  a  soft,  fleshy,  rapidly 
growing  growth,  called  the 
round  -  celled  sarcoma.  As 
cells  expend  their  \^tal  energy 
in  three  ways  (nutritive,  func- 
tional, and  reproductive  ac- 
tivity), the  embryonic  cells 
of  such  a  growth  may  ex- 
pend their  energy  in  nutrition 
(growth),  and  will  then  grow 
out    of    the   indifferent   stage 

into  a  more  mature  form  of  connective  tissue,  the  ultimate  form  of 
one  type  being  a  fibre,  an  embryonic  round  cell  undergoing  a  series  of 
form  changes  from  a  small  round  cell  to  a  long  fibre  (Fig.  30).  The 
growth  may  cease  at  any  stage  of  this  form  change,  the  timior  composed 
of  such  cell  forms  recei\dng  a  corresponding  name.  The  embryonic 
connective-tissue  tumors,  as  stated,  are  called  sarcomas,  the  form 
of  the  cells  composing  them  giving  them  a  qualifying  title. 


Porcine  embi-j-o  :  ct.  embryonic  connective  tissue 
of  mesoblast.     2y.2  cm.  X  2-50. 


Fig.  -30. 


®         @ 


In  Fig.  30  are  represented  the  stages  of  development  of  a  connective- 
tissue  fibre  from  a  round  cell.  If  growth  cease  at  stage  1,  and  the  cell 
energy  thereafter  expend  itself  in  reproduction,  a  rapidly  groTvdng 
tumor  composed  of  small  round  cells  is  formed — a  small  round-cell 
sarcoma,  markedly  malignant.  If  the  cells  expend  a  portion  of  energy 
in  growth  of  cell  size,  a  large-cell  sarcoma  is  formed,  less  malignant  than 
the  former.  If  the  cells  expend  a  portion  of  their  energy  in  forming 
intercellular  substance,  reproduction  and  malignancy  are  less  active. 
So  the  spindle  forms,  3  and  4,  represent  less  rapid  reproduction  and 


58 


DISTURBANCES  OF  NUTRITION. 


lesser  inalignancy  than  1  and  2,  although  the  form  4,  which  should  be 
of  less  rapid  reproduction  than  3,  because  of  more  mature  organization, 
is  frequently  more  malignant,  because  less  intercellular  substance  is 
formed,  as  shown  in  Figs.  31  and  32,  the  energy  represented  in  that 


Fig.  32. 


Fin.  31. — Small  spiiulle-cellcfl  sartuniii  i from  a  tumor  of  the  leg;).     X  200. 

Fig.  32. — Large  si)iiidle-cellofl  sarcoma.  To  tlie  left  the  cells  have  been  i<eparatecl  by  teasing, 
so  that  their  individual  forms  are  apijarent:  to  the  rig-ht,  they  are  in  their  natural  state  of 
apposition,  such  as  would  Ije  seen  in  a  thin  section  of  the  tumor.     ( Virehow.) 

process  being  used  up  in  reproduction.  The  nearer  the  approach  to  the 
mature  form  (6,  Fig.  30),  the  slower  the  growth  of  the  tumor,  which, 
when  composed  of  tissue  of  this  type,  loses  its  fleshy  (sarcomatous) 
appearance  and  becomes  fibrous,  and  is  hence  called  a  fibroma. 


G 


Fig.  33. 


^'q 


,vj>V 


-'it 


.■;. 


Myeloid  epulis  from  lower  ja'iv:  a,  multi- 
nucleated giant  cells;  h.  oval  cell.  '/  2i)r>. 
(Pepper.) 


Adenoma  of  the  breast :  a,  group  of 
glandular  acini;  6,  fibrous  stroma;  c,  cells 
broken  away  from  their  attachment.  X 
26.5.     (Pepper.) 


WTien  a  sarcoma  begins  its  growth  from  bone  its  histological  char- 
acter is  frequently  modified  (Fig.  33).  It  contains  large  marrow  cells 
which  have  undergone  incomplete  reproduction,  forming  giant  multi- 


EXCESS  OF  NUTRITION.     HYPERNUTBITION.  59 

nucleated  cells;  this  is  a  common  form  of  tumor  emerging  from  the 
sockets  of  teeth.  Some  of  the  cells  of  a  sarcomatous  growth  may  go  on 
to  maturity,  while  others  remain  at  some  stage  of  their  developmental 
career.  Malignancy  will  be  modified  according  to  the  amount  of 
mature  tissue  formed. 

Epithelial  Tumors.  Growths  arising  from  epiblastic  or  hypoblastic 
tissues  may  be  benign  or  malignant.  ^^Tiat  are  called  the  adenomata 
may  be  taken  as  the  type  of  the  benign  epithelioma;  that  is,  compara- 
tively benign.  They  present  all  of  the  characters  of  typical  glandular 
tissue:  numerous  acini  lined  with  epithelial  cells  and  surrounded  by 
connective  tissue  (Fig.  34).  Tumors  of  this  type  may  lose  their  com- 
parative benignancy  and  become  of  the  succeeding  epithelial  type. 

Carcinomata.  These  are  growths  arising  from  pre-existing  epithelial 
tissue,  which  possess  the  characteristics  of  epithelium  developing  with- 
out the  limitations  of  a  basement  mem- 

u  r>      •       •  1  •  *  Fig  35 

brane.   Joegmmng  upon  a  skm,  or  mucous  _.^    , 

surface,  or  in  a   gland,  the   reproduced        ^^      "  ^ 

epithelial  cells  are  not  sharply  marked  off  '^] 

from  the  connective  tissue  by  a  limiting    v 

membrane,  but,  gaining  entrance  to  the    V 

alveoli  of  connective  tissue,  they  prolifer-  '' 

ate  there,  find  their  way  into  lymphatic  1 

vessels  and  lymphatic  glands,  and  repro-      \  , 

duce  epithelial  growths  in  such  places  of  ~^  ] 

lodgement,  so  that  a  tumor  having  its  "  " 

origin  in  one  part  may  give  rise  to  tumors  ^  _  ^ 

in  other  parts  of   the   bodv — metastasis 

.-p,.  ,  ^  Section  through  an  aggregation  of 

V-Tlg.  OOJ.  very  young  cancer  cells,  lodged  like 

Like     the    connective-tissue     tumors,    ;»»  embolus  withm  a  capiuary  of  the 

'     liver.      The   loarent    growth  was  an 

types    of    carcinoma    differ   as    to    rapidity     adenocarcinoma     of     the     stomach. 

n  ji     •       n      •  ••!•,        ■•  1      Preparation  stained  -with  hsematox- 

ot  growth  m  their  original  situation  and    j-nn.   x  300.    (ziegier.) 
in  the  degree  of  transference;  these  fac- 
tors determine  their  malignancy.    Tumors  of  the  sarcoma  group  may 
also  give  rise  to  growths  in  other  parts,  the  tumor  cells  being  carried 
thence  by  lymphvessels  or  bloodvessels. 

After  a  period,  tumors  frequently  suffer  such  interference  with  their 
nutrition  that  degeneration  occurs  in  them. 

After  removal,  some  varieties  of  tumors,  both  those  which  infiltrate 
surrounding  tissues  and  those  which  are  metastatic,  show  a  tendency  to 
recurrence;  that  is,  removal  does  not  effect  a  cure,  and  the  tumor 


60  DISTURBANCES  OF  NUTRITION. 

may  upon  reappearance  assume  another  and  a  more  malignant  char- 
acter. 

Epithelial  tumors  never  become  tumors  of  the  connective-tissue 
type;  and,  vice  versa,  connective-tissue  tumors  cannot  become  epithelial 
tumors. 

The  distinction  formed  between  epiblast  and  mesoblast  in  the 
embryo  is  maintained  throughout  life. 


DEFICIENCY  OF  NUTRITION.     HYPONUTRITION. 

If  the  quantity  or  quality  of  the  blood  delivered  to  a  part  be  deficient, 
the  nutrition  of  the  cells  of  the  part  is  impaired.  First,  atony,  a  lessened 
activity  of  the  vital  processes  of  the  part,  occurs.  Cell  chemistry  is  dis- 
ordered, less  oxidation  occurs,  hence  there  is  a  lessened  heat  produc- 
tion. 

The  function  of  the  cells  is  diminished:  if  secretory,  its  secretion 
is  lessened;  if  muscular,  the  cell  has  a  lessened-  contractility;  the 
relations  between  nutrition  and  waste  are  disturbed;  the  part  becomes 
physiologically  wearied  sooner  than  usual. 


Adipose  tissue.    A,  noi-mal;  B,  atrophic,  from  a  ease  of  phthisis;  a,  a  single  fat-cell,  with  cell 
wall,  nucleus,  and  drop  of  fat.     X  300.     (Virchow.) 

If  the  process  cause  interference  with  the  development  of  an  organ, 
so  that  it  is  much  below  normal  in  size,  the  condition  is  spoken  of  as 
aplasia  or  agenesia. 

If  the  interference  merely  checks  the  growth  of  a  developed  organ, 
the  condition  is  known  as  hypoplasia. 

Atrophy.  If  the  process  of  hyponutrition  be  marked,  the  waste  in 
the  part  may  exceed  repair,  and  the  part  affected  becomes  diminished 
in  size  or  atrophied.  Atrophy  may  be  general  or  local.  In  general 
atrophy  there  is  a  general  loss  of  tissue  due  to  an  excessive  waste  or 


DEFICIENCY  OF  NUTRITION.    HYPONUTRITION.  61 

faulty  assimilation  of  food  by  the  tissues.  There  is  a  loss  of  bodily 
weight,  due  first  to  a  loss  of  the  fat,  later  to  shrinkage  in  the  tissue 
cells.  The  shrinkage  in  size  of  the  tissue  cells  causes  shrinkage  of  the 
entire  organ.  The  cells  may  recover  their  size  when  the  faulty  waste 
or  assimilation  is  corrected.  During  atrophy  many  cells  are  lost 
through  the  process  of  fatty  degeneration  and  removed  by  the  phago- 
cytes (leukocytes),  so  that  atrophy  may,  like  hypertrophy,  be  both 
simple  and  numerical.  An  atrophied  part  is  pale  and  shrunken,  con- 
tains less  fluid,  and  is  tough  and 

Fig    37 

fibrous.   At  times  the  fibrous  por- 
tion  or  connective  tissue  may  m-  ? , 

crease  as  the  cells  diminish  (scle-  ^ 

rosis).  ' 

Causes.       General    atrophv   is  ,»    ^  i         - 

caused:^    1.  By  a  deficient  supply         ^        3/   ^         '  >  '. 

of  food  material  delivered  to  the 

tissue   cells.     This   may  be  due  ' 

to  a  primary  food  deficiency  or  ( 

any  interference  with  its   prepa-  '       h  1 

ration  for  absorption  or  with  its  i^^i  -    *     I  [     I  -    Pf/ 

proper  absorption  or  circulation.         '        [     , 
2.  By  excessive  waste  of  the  tis-        '^^  1 

sues  generally,  as  in  fevers,  pro-        f      «  / 
longed  suppuration,  etc.    3.   By        I      ^sa     ^, 
impaired  vital  activity  of  the  cells        j       'jj*        ^  I    ^  '  \ 

themselves,  as  in  senile  conditions.        I"     f  e  |  '  fl  ^  pi 

Local  atrophy  may  be  caused:       *rT---l®C2(  >  1^ '/^|, >  i|  '   9 

1.  By  a  lessened  circulation  in  a    -,     ,   „,  .     ,       '  , 

•/  Muscle  nbres  in  simple  atrophy.     (Sehmaus.) 

part  due  to   obstruction    of   the 

arteries,  veins,  or  capillaries.  2.  By  diminished  functional  activity  or 
disuse  of  a  part,  as  in  the  case  of  unused  muscles  or  even  bones. 
Certain  organs  are  atrophied  or  resorbed  as  a  part  of  the  cycle  of 
life — e,  g. ,  the  umbilical  cord,  the  roots  of  deciduous  teeth,  the  thymus 
gland,  the  mammary  glands  after  the  menopause.  3.  The  loss  of 
nervous  connection  of  a  part  with  the  nerve  centres  controlling  it 
(trophoneurosis).  4.  Excessive  functional  activity  may  cause  atrophy 
by  producing  a  degenerative  condition  due  to  overstimulation. 

1  Green. 


/         I 


62  DISTURBANCES  OF  NUTRITION 


MALNUTRITION. 


By  the  term  malnutrition  is  meant  a  more  or  less  general  disturbance 
of  the  metabolism  of  cells,  as  a  result  of  the  failure  of  one  or  more 
important  organs  to  perform  its  full  function,  either  of  food  supply  or 
waste  elimination.  The  fault  may  lie  with  disturbance  of  the  nervous 
system  controlling  metabolism  or  with  the  stomach,  lungs,  liver,  skin, 
kidney,  blood,  etc.  The  tissues  are  either  deprived  of  normal  food 
elements  (tissue  starvation)  or  are  presented  with  waste  products 
formed  within  the  body  and  retained  in  the  blood  (auto-intoxi- 
cation). The  proteids  of  which  the  tissues  are  normally  composed 
are  not  normally  built  up,  and  a  general  disease  of  the  cellular 
elements  of  the  body  occurs.  These  lose  their  vital  potential  and 
capacity  for  resistance  to  other  forms  of  exciting  causes,  such  as 
bacteria.  Whether  a  tangible  disease  condition  or  merely  an  altera- 
tion in  nutrition  not  obvious  to  the  individual,  it  may  act  as  a  predis- 
position to  local  bacterial  action — e.  g.,  as  in  pyorrhoea  alveolaris. 
When  the  malnutrition  is  accompanied  by  a  local  infection,  the  latter 
may,  by  the  production  of  toxins  which  are  absorbed,  increase  the 
malnutrition,  which  further  aids  the  action  of  the  exciting  causes  by 
acting  as  a  predisponent,  lessening  resistance.  This  result  is  called  a 
\icious  circle.     (See  Pyorrhoea  Alveolaris.) 

DEGENERATION. 

If  cells  have  reached  the  limit  of  their  life  cycle  or  have  been  sub- 
jected to  influences  markedly  disturbing  their  nutrition,  the  proteids 
of  which  they  are  composed  are  replaced  by  other  substances  formed 
from  the  cell  proteids  and  accumulated  at  their  expense.  As  a  rule, 
the  cells  shrink  in  size  and  number,  so  that  atrophy  usually  is  asso- 
ciated with  degeneration.  This  is  a  true  degeneration,  and  is  to  be 
distinguished  from  an  infiltration  of  foreign  material  into  a  cell,  which 
material  mechanically  pushes  aside  the  cell  protoplasm — e.g.,  fat- 
globules  in  liver  cells  ('Fig.  38). 

Fatty  Degeneration.  Fatty  degeneration  is  a  condition  in  which 
an  accumulation  of  fat  is  found  in  the  substance  of  cells  as  the  result 
of  partial  decomposition  of  cell  substance  itself.  The  cell  appears 
granular  and  fat-droplets  appear  within  the  substance  of  the  proto- 
plasm.   These  do  not  tend  to  coalesce,  as  in  the  case  of  fat  infiltration. 


DEFICIENCY  OF  NUTRITION.    DEGENERATION. 


63 


"The  larger  the  amount  of  cell  albumin  replaced  by  fat,  the  nearer 
is  the  whole  cell  to  death."  (Fig.  40). 

Causes. — Depression  of  the  vital  activity  of  the  cells  is  always  the 
proximate  cause.  This  maybe  induced  (1)  by  an  altered  blood  supply 
or  a  persistent  diminution  in  the  supply  of  oxygen  to  the  cells;  (2)  by 
changes  in  the  physical  condition  of  the  cells,  or  (3j  by  an  expression 
of  the  natural  limit  of   life  of  the  cells.     Of  these  causes,  probably 


Fig. 


Fig.  39. 


-^^^'        'i^hsi  /SFVk 

"^  W   0 


Liver  cells  in  vai-ious  stages  of  fatty 
accumulation.     X  300.     (Rindfleisch.) 


Fatty  degeneration  of  cells:   a,  from  a  cancer;    6, 
from  the  brain  in  chronic  softening.     \'  200.    (Green.) 


Fig.  40. 


t»   SJV'.. 


-^f~ 


■.-i^«aB»«>* 


■^■•^ ' "-' 


:>^ 


^^rjtgSS^ 


u*-^'i^^"'-*-^** 


sl:^^- 


Fatty  degeneration  of  the  heart,  from  a  case  of  isernicious  anaemia.  The  protoplasm^is 
replaced  by  globules  of  various  .sizes  stained  black  by  osmic  acid.  The  outlines  of  the  fibres 
are  irregular  o'wing  to  inequality  in  their  distention.     X  400.     (Green.) 

the  insufficiency  of-  oxygen  supplied,  as,  for  example,  in  anaemia  or 
in  inflammation,  or  the  inability  of  the  cell  to  appropriate  oxygen 
seems  to  be  the  most  important  factor  (Fig.  40).  In  inflammation 
the  oxidation  of  cells  is  interfered  with,  and   fatty  degeneration  of 


^  Green,  Pathology  and  >Iorbid  Anatomy. 


64  DISTURBANCES  OF  NUTRITION. 

cells  occurs.  In  areas  which  have  undergone  fatty  degeneration,  a 
cheesy  substance  may  be  formed  out  of  the  degenerated  elements 
existing  in  the  part.  The  fluid  is  gradually  absorbed  and  a  mass 
composed  of  atrophied  cells,  fatty  debris,  and  cholesterin  crystals  is 
left.  This  process  is  known  as  caseation.  Encapsulation  of  the 
caseous  mass  by  fibrous  tissue  may  take  place,  or  its  liquefaction 
or  its  calcification  may  occur.  Fatty  degeneration  may  occur  in  many 
tissues,  and  the  danger  is  proportionate  to  the  importance  of  the 
tissue  involved. 

Cloudy  Swelling  {Parenchymatous  or  Granular  Degeneration). 
Cloudy  swelling  is  a  change  occurring  in  the  parenchyma  (essential 
cells)  of  a  part  as  the  result  of  the  presence  of  toxic  substances  in  the 
blood. 


.,^>  '■ 


I  ^.<-.-r^,  ...  ■,•._■..-,-.•  >  .  .,■.. 


.■0ff-^ 


ar-~—ip 


t 


-V  - 


Cloudy  swelling  of  kiilney  epithelium:  a,  normal  eijithelium  :  b.  epithelium  beginning  to  be 
cloudy ;  c,  advanced  degeneration  ;  d,  cast-off  degenerated  epithelial  cells.  From  a  preparation 
■which  had  been  treated  with  ammonium  chromate.     X  600.     (Ziegler.) 

Causes.  The  toxins  of  the  acute  specific  fevers  and  also  phosphorus, 
arsenic,  and  the  mineral  acids  act  as  causes. 

Pathology.  The  cell  absorbs  fluid,  swells,  its  contents  become  gran- 
ular, and  the  histological  structure  is  lost.  In  the  early  stages  the 
change  is  albuminous;  no  fat  is  demonstrable;  later,  however,  it 
appears,  so  that  the  change  is  regarded  as  a  first  stage  in  the  produc- 


DEFICIENCY  OF  NUTRITION.    DEGENERATION. 


65 


tion  of  fatty  degeneration,  by  which  process  many  of  the  cells  are  lost, 
though  the  organ  may  recover  if  the  patient  withstands  the  original 
disease  (Fig.  41). 

Mucoid,  Colloid,  and  Hyaline  Degeneration.  The  albumin  of 
cells  may  undergo  other  chemical  changes  than  transformation  into 
fatty  substances;  they  may  undergo  mucoid,  colloid,  or  hyaline  trans- 
formation. The  causes  of  the  degeneration  are  not  made  out.  The 
function  of  the  part  affected  is  destroyed. 

Lardaceous  Degeneration.  This  type  of  degeneration  is  known 
as  amyloid,  albuminous,  or  waxy.  The  formation  of  the  material  from 
which  this  condition  derives  its  name  is  preceded  by  an  unknown  type 


Fig.  42. 


o'^.'°<^^ 


■^1 


'^Sr^Tf^ 


.:^,'^ 


x^^-t*^ 


mM3>£^ 


Calcareous  infiltration  of  renal  epithelia.     From  the  edge  of  an  old  infarct ;  a  few  tubules  still 
to  be  recognized.     X  2.50.     (Schmaus  and  Ewing.) 


of  degeneration  of  the  cells  of  the  part  affected.  The  degenerative 
processes  appear  to  be  the  result  of  long-continued  suppuration  due 
usually  to  tubercular  diseases.  In  the  connective  tissue  about  the 
degenerated  cells  a  substance  akin  to  albumin  is  deposited,  which 
causes  swelling  and. a  pseudohypertrophy  of  the  organ  affected.  The 
substance  gives  a  reaction  with  iodine  resembling  that  of  starch;  hence 
the  name  amyloid  {amylum,  starch).  It  may  affect  any  organ  of  the 
body.  It  usually  appears  first  in  the  connective  tissue  lying  between 
the  inner  and  middle  coats  of  small  arteries.  The  swelling  caused  by 
the  infiltration  markedly  lessens  the  calibre  of  the  vessels  and  diminishes 


66  DISTURBANCES  OF  NUTRITION 

the  nutritive  supply  of  the  parts  suppHed  by  the  artery,  which  may  lead 
to  fatty  degeneration  and  atrophy  of  the  insufficiently  nourished  parts. 

Calcareous  Degeneration.  In  tissues  which  have  undergone  pre- 
vious degeneration,  calcium,  sodium,  or  magnesium  salts  may  be 
deposited  as  an  infiltration  from  the  blood  plasma.  The  parts  are 
thus  petrified.    The  cells  take  no  active  part  in  the  process.^ 

It  is  believed,  however,  that  the  deposit  of  salts  in  the  d^dng  tissue 
is  more  than  a  mere  precipitation,  and  that  calcification  results  from  a 
combination  of  the  salts  with  an  albuminous  base  and  with  fatty  acids, 
such  an  affinity  being  favored  by  the  degenerative  changes.  Ordinarily 
the  carbonate  and  phosphate  of  calcium  are  the  infiltrating  salts,  but 
in  gout  uric  acid  salts  are  deposited,  owing  to  an  excess  of  uric  acid 
in  the  form  of  urates  in  the  body  fluids.  A  sluggish  circulation  in  the 
part  favors  the  deposition  of  the  salts.  The  calcification  may  occur 
in  both  the  cells  and  in  the  intercellular  substance."  (See  Calcific 
Degeneration  of  the  Pulp.) 

"The  white  fibrous  tissue  is  the  form  of  connective  tissue  usually 
affected,  but  concretions  may  occur  in  the  connective  tissue  surrounding 
the  bloodvessels."^ 

As  a  secondary  process  after  degeneration,  calcification  of  the  middle 
coats  of  the  arteries  may  occur,  rendering  them  inelastic.  This  renders 
them  incapable  of  regulating  the  blood  supply  to  parts,  and  these  suffer 
more  or  less  nutritive  disturbance,  and,  in  some  cases,  actual  death 
of  the  part  (gangrene).  Many  forms  of  free  calculi  are  formed  in  the 
body.  These  occur  most  frequently  in  ducts  or  ca^dties  lined  with 
epithelium — e.  g.,  the  salivary  ducts  and  the  bladder. 

"All  free  concretions  have  an  organic  basis  or  nucleus,"  with  which 
is  combined  the  calcium  salts,  oxalates,  cholesterin,  etc.,  making  up  the 
inorganic  or  crystallizable  part  of  the  combination.  The  organic  part 
may  consist  of  inspissated  feces,  as  in  enteroliths;  mucus  or  mucin,  as 
in  the  calculi  upon  the  teeth;  epithelial  scales,  mucus,  etc.,  in  the 
urinary  passages.* 

Calcareous  degeneration  is  clearly  to  be  distinguished  from  the 
normal  calcification  of  the  hard  tissues,  bone,  enamel,  dentine,  and 
cementum.  These  are  composed  of  calcoglobulin,  in  which  calcium 
and  magnesium  salts  are  combined  under  the  superintendence  of 
certain  li\ang  cells  with  albuminous  bases  derived  probably  from  their 
own  substance. 

1  Green,  Patholog>-  and  Morbid  Anatomy.  -  Ziegler,  General  Pathology. 

3  Ibid.  *  Ibid. 


DEFICIENCY  OF  NUTRITION.    NECROSIS.  67 

NECROSIS. 

Necrosis  (from  nekros,  dead)  signifies  death  in  mass  of  a  part  due 
to  a  profound  disturbance  in  its  nutritive  supply  or  to  a  destruction  of 
the  vital  activity  of  its  cellular  elements. 

Causes.  The  conditions  which  bring  about  a  cessation  of  vitality 
in  the  cells  of  tissues  may,  therefore,  be  grouped  under  two  heads: 
1.  Interference  with  the  supply  of  nutritive  material.  2.  Destruction 
of  the  vital  activity  of  the  cellular  elements. 

Class  I.  An  interference  with  the  nutritive  supply  of  cells  through 
obstruction  in  the  arteries,  capillaries,  or  veins  is  the  usual  cause. 

1.  Obstruction  of  the  Arteries.  If  from  any  cause — surgical  ligation 
of  an  artery,  pressure  upon  it  by  effusion  or  new-growths,  degenera- 
tion or  affections  of  the  arterial  walls,  the  presence  of  an  embolus 
or  thrombus — the  flow  of  blood  to  a  part  is  arrested,  the  nutritive 
supply  ceases  and  the  cells  dependent  upon  that  vessel  perish.  If  the 
part  receive  a  collateral  arterial  supply,  the  cells  may  retain  their 
vitality,  although  if  this  supply  be  inadequate  they  are  in  danger  of 
degeneration  and  atrophy.  This  will  explain  the  greater  relative  fre- 
quency of  extensive  necrosis  of  the  lower  jaw,  as  compared  with  necro- 
sis affecting  the  upper  jaw,  the  lower  jaw  being  supplied  mainly  by  one 
large  arterial  trunk,  while  in  the  upper  jaw  there  is  a  freely  anastomos- 
ing circulation. 

2.  Obstruction  of  the  Veins.  If  the  entire  venous  outlet  of  a  part 
be  obstructed,  there  is  not  that  removal  of  waste  products  necessary  to 
the  life  of  cells ;  moreover,  access  of  nutritive  material  is  prevented  and 
the  parts  die. 

3.  Obstruction  of  the  Capillaries.  Complete  obstruction  of  the 
capillary  supply  to  a  part  is  followed  necessarily  by  a  cessation  of  nutri- 
tion in  the  part;  consequently  necrosis  results.  For  example,  when  an 
inflammatory  effusion  occurs  between  the  surface  of  a  bone  and  the  peri- 
osteum, the  capillaries  are  torn  from  their  attachment;  and  if  the  condi- 
tion be  prolonged,  necrosis  of  the  underlying  bone  results.  When  the 
effusion  occurs  outside  the  periosteum  its  pressure  may  cause  occlusion 
of  the  capillaries  of  the  part.  The  interference  with  the  nutritive  supply 
may  be  due  to  a  lack  of  force  with  which  the  blood  is  propelled,  owing 
to  insufficient  action  of  the  heart.  Necrosis  is  not  infrequently  due  to 
the  violence  and  continuance  of  the  inflammatory  process  in  a  part. 
Coagulation  of  the  blood  in  the  capillaries  of  a  part  occludes  the  circu- 
lation and  death  results. 


68  DISTURBAXCES  OF  NUTRITION. 

Class  II.  Destruction  of  the  vital  activities  of  cells  may  be  caused 
by  any  of  the  physical  forces  or  by  the  action  of  chemical  agents, 
including  among  the  latter  the  poisonous  substances  formed  through 
the  action  of  bacteria. 

Injuries,  blows,  excessive  heat  or  cold,  the  passage  of  powerful  elec- 
tric currents,  are  all  influences  which  directly  injure  or  permanently 
destroy  vital  activities  of  cells.  The  application  of  chemical  agents 
which  so  act  upon  cell  substance  as  to  change  its  character  produces 
necrosis. 

AVhile  this  is  particularly  true  of  such  substances  as  powerful  acids 
and  alkalies,  which  immediately  destroy  cell  integrity,  it  is  also  true 
of  milder  agents  acting  for  longer  periods.  Certain  poisons,  par- 
ticularly those  of  bacterial  origin,  paralyze  the  vital  activities  of  cells 
and  necrosis  results. 

The  occurrence  or  non-occurrence  or  the  liability  to  necrosis  will 
largely  depend  upon  the  degree  of  vital  energy  of  cells  prior  to  the 
action  of  the  active  causes  of  necrosis.  Parts  debilitated  from  any 
cause  are  more  liable  to  necrosis  than  those  which  have  suffered  no 
debility.  A  part  chronically  ill-nourished  subjected  to  the  causes 
producing  degenerations  is  liable  to  suffer  necrotic  changes,  for  the 
several  degenerations  and  atrophy,  are  but  successive  stages  leading 
to  necrosis. 

AMien  a  tissue  undergoes  death  as  the  result  of  the  infliction  of  an 
injury  the  process  is  called  necrosis  per  se,  to  distinguish  it  from  the 
form  of  death  which  occurs  in  a  descending  scale,  which  process  is 
called  necrobiosis. 

A  necrosed  part  acts  as  an  irritant  to  the  tissues  about  it,  inau- 
gurating an  inflammatory  reaction  which  marks  off  the  dead  from 
the  li\-ing  parts.  The  dead  part  is  sequestered,  and  hence  is  called  a 
sec[uestrum. 

Necrosis  may  be  of  several  types,  of  which  the  following  are  the 
chief  forms: 

Coagulation  Necrosis.  When  a  dead  tissue  contains  coagulable 
material  and  the  necessary  ferments  the  parts  undergo  coagulation. 
(See  Coagulation.)  The  cells  and  parts  about  become  solidified; 
the  cells  lose  their  nuclei  and  do  not  stain  as  usual.  It  occurs  in 
suppuration. 

Liquefaction  Necrosis.  When  the  necrosed  parts  are  saturated 
with  l\Tnph  the  dead  part  breaks  down  and  liquefies. 


DEFICIENCY  OF  NUTRITION.     GANGRENE. 


69 


GANGRENE. 


When  death  en  masse  of  a  part  occurs  as  the  resiiU  of  an  interference 
with  its  nutritive  supply  the  process  is  termed  gangrene. 


Fig.  43. 


a^ 


Senile  gangrene  of  the  great  toe,  from  a  case  of  arterial  thronibosi-s.  The  toe  is  shrunken 
and  its  epidermis  is  being  exfoliated.  At  the  line  of  demarcation  the  skin  has  retracted  (a) 
and  the  deeper  parts  are  separating  (6).     (Green.) 

Dry  Gangrene.  In  parts  which  ordinarily  contain  but  little  fluid 
the  obstruction  of  the  artery  may  be  associated  with  but  little  obstruc- 
tion of  the  veins  and  lymphatics.  Under  such  circumstances  the  dead 
part  is  drained  of  the  little  fluid  it  contains  and  a  fresh  access  of  fluid 


Dry  gangrene  of  the  toes,  caused  by  narrowing  and  closure  of  the  arteries  supplying  these 
parts — arteriosclerosis.     ( Ziegler.) 

is  prevented.  Exposure  to  the  air  aids  a  further  loss  of  moisture  by 
evaporation.  The  conditions  are  not  favorable  to  the  development  of 
micro-organisms  and  the  part  changes  from  a  pale  appearance  to  a 


70  DISTURBANCES  OF  NUTRITION. 

dark,  shrunken  one.  The  process  of  grackial  drying  is  also  called 
mummification.     (See  Dry  Gangrene  of  the  Pulp.) 

Moist  Gangrene.  Under  opposite  conditions  —  i.e.,  a  venous 
obstruction  with  a  weak  arterial  supply — there  is  much  venous 
engorgement  and  extravasation  of  blood  into  the  tissues,  which  are 
stained  red  by  the  haemoglobin  from  disintegrated  red  corpuscles. 
Abundant  effusions  also  cause  the  part  to  be  swollen.  Death  of  tissue 
occurs  from  interference  with  nutrition.  The  moisture  present  favors 
the  development  of  bacteria  and  they  enter  the  tissue  through  the 
skin.  Putrefaction  wdth  the  evolution  of  malodorous  gases,  such  as 
hydrogen  sulphide  (HjS),  hydrogen  phosphide  (PH3),  and  ammonium 
sulphide  (NH^)„S,  causes  the  part  to  have  an  offensive  odor. 

If  the  gangrene  be  due  to  infective  inflammation  or  the  surrounding 
tissue  be  debilitated  from  any  cause,  the  area  of  gangrene  may  spread 
— i.  e.,  invade  the  living  tissue  (spreading  gangrene).  This  is  probably 
due  to  the  presence  of  bacteria,  which  irritate  and  progressively  destroy 
the  surrounding  tissue.  If  the  adjacent  tissue  be  healthy  and  resistant, 
a  line  of  demarcation  is  established,  consisting  of  leukocytes,  which 
dissolve  all  fibres  or  firm  connections  between  the  dead  and  living 
parts.  Suppuration  occurs  at  the  line,  and  the  dead  portion  is  separated 
as  a  sphacelus  or  slough.  Occurring  in  bone  this  is  called  a  sequestrum. 
An  ulcerated  surface  is  left.  The  latter  form  is  circumscribed  gan- 
grene. If  gangrene  be  deep-seated  and  septic,  suppuration  occurs, 
which  establishes  one  or  more  fistulse  upon  the  surface  of  the  body  or 
in  one  of  its  ca\aties.  (See  Moist  Gangrene  of  the  Pulp.)  A  seques- 
trum may  be  cast  out  through  one  of  these.  In  the  aged  atheromatous 
or  calcareous  changes  in  the  arteries  produce  a  slow  circulation  in  the 
extremities.  A  slight  injury  to  a  vessel  wall  may  induce  extensive 
thrombosis  (which  see).  The  result  is  gangrene  of  a  part  or  all  of  an 
extremity  known  as  senile  gangrene  (Fig.  43). 


CHAPTER   V. 


DISTURBANCES  OF  THE  VASCULAE  SYSTEM. 


A  CERTAIN  amount  and  quality  of  blood  flows  through  the  circulatory 
apparatus  and  is  in  close  relation  to  processes  of  nutrition. 

The  amount  of  blood  in  the  vessels  may  be  increased  (plethora). 
It  may  be  decreased  in  quantity  or  its  red  corpuscles  may  be  lessened 
in  number  (anaemia).  The  proportion  of  white  corpuscles  to  red  ones 
may  be  increased  abnormally  (leukaemia).  The  haemoglobin  of  red 
corpuscles  may  be  deficient  (chlorosis).  Locally  the  amount  of  blood 
in  a  part  may  be  increased  (hypereemia  or  inflammation)  or  diminished 
(ischsemia). 

Normally  the  blood  contains  floating  in  the  plasma  5,000,000  red 
corpuscles  or  erythrocytes  and  from  5000  to  10,000  (1  to  500  red) 
white  corpuscles  or  leukocytes  to  each  cubic  millimetre.  (See  Plate  I., 
Fig  2.)  A  marked  increase  in  the  number  of  erythrocytes  is  termed 
polycythsemia ;  a  marked  decrease  oligocythsemia.  The  temporary 
increase  in  number  of  white  corpuscles  is  leukocytosis;  a  persistent 
increase  leukocytheemia  or  leukaemia. 

The  blood  corpuscles  may  be  classified  as  follows: 


Erythrocytes. 
Non-nucleated 
red  corpuscles. 


Erythroblasts. 

Nucleated  red  corpuscles 

derived  from  red  marrow 

of  bones. 


Leukocytes. 
White  corpuscles. 


Normal  to 
blood. 

Pathological 
indicators. 


■!    Pathological 
j       indicators. 


r  Normal  to 
blood. 


Pathological 
indicators. 


Normocytes  (normal  size), 


Plate  I. 

Fig.  45. 

Fig.  7. 

1,  2,  3.  4. 

a 

Microcytes  (small  size). 
Macrocyte  (large  size). 
Megalocyte  (very  large  size) , 
[  Poikilocyte  (irregular  form). 


r  Normoblasts  (normal  size) 
\    Microblasts  (small  size) 
[  Megaloblasts  (large  size) 


(  Lymphocyte,  small 


J    Lymphocyte,  large  . 

I    Polymorphonuclear  neutrophiles  70 

I  Polymorphonuclear  eosinophiles .  2 


Fig.  45, 
22%    5 
,  6  "      6 

7 


defg 


Plate  L 

Fig.l 
/ 


Basophilic  leukocytes  or  mast-cells. 
Neutrophilic  myelocytes  from  bone-marrow 
[  Eosinophilic  myelocytes         .... 


72 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


Fic.   1." 


Normal  blood  (triacid  stain).  1.  Normal  red  cell,  flatly  spread  and  evenly  stained.  2. 
Normal'rouleau.  3.  Normal  red  cells  varying  slightly  in  size,  thickly  spread,  showing  centi'al 
clear  areas.  4.  Normal  red  cell,  of  slightly  altered  shape.  5.  Lymphocyte,  medium  size.  6. 
L/arge  mononuclear  leukocyte,  incurved  nucleus.  7.  Polynuclear  neutrophyle  leukocyte.  8. 
Eosinophile  leukocyte.     Separate  nuclear  lobes.     (Schmaus  and  Ewing.l 


ANEMIA. 

Ansemia  is  a  condition  in  which  the  blood  is  lessened  in  quantity  or 
partly  deprived  of  its  essential  constituents — i.e.,  red  corpuscles  and 
haemoglobin — in  consequence  of  which  the  tissues  receive  less  oxygen 
and  the  general  nutrition  is  impaired. 

Acute  traumatic  anaemia  occurs  as  a  result  of  copious  hemorrhage. 
The  individual  becomes  temporarily  pale  and  weak.  The  arterial 
pressure  is  lessened,  the  circulation  slowed,  and  the  pulse  is  frequent 
and  small.  Recovery  is,  as  a  rule,  prompt,  the  water  being  first 
restored  and  later  the  corpuscles  being  regenerated.^  Frequent  hemor- 
rhages cause  the  blood  to  become  watery,  and  debility  results  from 
impaired  nutrition.     (See  Plate  I.,  Fig.  3.) 


1  Ziegler,  General  Pathology. 


Fi^/ 


FiffH. 


FigUJ 


Fty.Vm. 


6 

c 

d 

f  c 

i 

J 

/• 

/ 

m 

n 

^  % 

A 

0 

s 

# 

&  ^ 

M 

^ 

BLOOD. 

(Ehrlich  triple  stain.) 
(Prepared  by  Dr.  I.  P.  Lyon.) 

f'ig.  I.     TYPES   OF    LEUCOCYTES. 

o.  Polymorphonuclear  Neutrophile.  6.  Polymorphonuclear  Eosinophile.  c.  Myelocyte 
(Neutrophilic),  d.  Eosinophilic  Myelocyte,  e.  Large  Lymphocyte  (large  Mononuclear). 
/.  Small  Lymphocyte  (small  Mononuclear). 

Fig.  II.     NORMAL   BLOOD. 
Field  contains  one  neutrophile.     Reds  are  normal. 

Fig.  III.     ANEMIA,   POST-OPER.\TIVE  (secondary). 

The  reds  are  fewer  than  normal,  and  are  deficient  in  haemoglobin  and  somewhat 
irregular  in  form.  One  normoblast  is  seen  in  the  iield,  and  two  neutrophiles  and  one 
small  lymphocyte,  showing  a  marked  post-hsemorrhagic  anaemia,  with  leucoeytosis. 

Fig.  IV.     LEUCOCYTOSIS,  INFLAMMATORY. 

The  reds  are  normal.  A  marked  leucoeytosis  is  shown,  with  five  neutrophiles  and 
one  small  lymphocyte.  This  illustration  may  also  serve  the  purpose  of  show^ing  the 
leucoeytosis  of  malignant  tumor. 

Fig.  V.     TRICHINOSIS. 
A  marked  leucoeytosis  is  shown,  consisting  of  an  eosinophilia. 

Fig.  VI.     LYMPHATIC  LEUKEMIA. 

Slight  anaemia.  A  large  relative  and  absolute  increase  of  the  lymphocytes  chiefly 
the  small  lymphocytes)  is  shown. 

Fig.  VII.     SPLENO-MYELOGENOUS   LEUKEMIA. 

The  reds  show  a  secondary  anaemia.  Two  normoblasts  are  shown.  The  leucoeytosis 
is  massive.  Twenty  leucocytes  are  shown,  consisting  of  nine  neutrophiles,  seven  myelo- 
cytes, two  small  lymphocytes,  one  eosinophile  (polymorphonuclear)  and  one  eosinophilic 
myelocyte.  Note  the  polymorphous  condition  of  the  leucocytes,  i.e.,  their  variations 
from  the  typical  in  size  and  form. 

Fig.  VIII.     VARIETIES   OF   RED    CORPUSCLES. 

a.  Normal  Red  Corpuscle  (normoeyte).  6,  c.  Anaemic  Red  Corpuscles,  d-g.  Poikilocytes. 
h.  Microsyte.  i.  Megalocyte.  J-n.  Nucleated  Red  Corpuscles.  j,k.  Normoblasts.  I.  Micro- 
blast,    m,  n.  Megaloblasts. 


ANEMIA.  73 

Symptomatic  Anaemia.  A  diminution  in  the  number  of  red  cor- 
puscles may  occur  as  a  result  of  protracted  overwork,  anxiety,  study, 
or  long-continued  illness,  such  as  a  fever. 

The  number  of  red  blood  corpuscles  may  be  reduced  to  one-half  the 
normal  amount,  and  there  is  a  corresponding  debility.  The  condition 
may  disappear  with  appropriate  removal  of  the  cause. 

Chlorosis.  This  is  a  form  of  anaemia  occurring,  for  the  most  part, 
in  girls  and  young  women,  and  characterized  by  a  great  deficiency  in 
the  haemoglobin  of  the  red  corpuscles  without  a  corresponding  reduc- 
tion in  the  number  of  the  red  corpuscles.  In  the  blood  very  small  red 
corpuscles  (microcytes)  are  seen;  also  a  few  very  large  ones  (macro- 
cytes),  and  some  of  irregular  outhne  (poikilocytes).^  The  pathology  is 
uncertain. 

Being,  as  a  rule,  readily  cured  by  a  course  of  iron,  it  is  inferred 
that  the  body  is  starved  of  iron,  an  essential  constituent  of  haemo- 
globin. It  is  often  associated  with  gastric  disturbances,  constipation, 
defective  hygiene,  and  irregular  habits,  which  apparently  have  a  causal 
relation.  The  skin  and  mucous  membranes  are  pale  and  have  a 
slightly  greenish  tinge  .^ 

Leukocytosis.  This  is  not  a  form  of  anaemia,  but  a  temporary 
increase  in  the  number  of  multinucleated  leukocytes,  apparently  derived 
from  the  lymphoid  structures  of  the  body  in  response  to  some  demand 
for  leukocytes.  Thus  it  occurs  after  a  full  meal,  in  the  later  months  of 
pregnancy,  in  acute  fevers,  in  tuberculosis,  and  in  conditions  accom- 
panied by  suppuration.^  Its  presence  during  the  course  of  surgical 
disease  has  been  held  to  be  diagnostic  of  pus  formation* — e.  g.,  in 
abdominal  surgery.     (See  Plate  I.,  Fig.  4.) 

Leukaemia.  Leukaemia  is  a  disease  characterized  by  a  considerable 
and  permanent  increase  in  the  number  of  white  corpuscles  of  the  blood, 
by  a  diminution  in  the  number  of  the  red  corpuscles,  and  by  enlarge- 
ment of  some  of  the  lymphatic  organs.  The  proportion  of  one  white 
to  ten  red  corpuscles  is  common.  The  spleen  may  be  hypertrophied 
(splenic  leukaemia).  The  lymphatic  glands  may  be  hypertrophied 
(lymphatic  leukaemia).  In  these  cases  the  blood  contains  an  excess 
of  uninuclear  leukocytes.  When  the  marrow  of  bones  is  hyper- 
trophied (myelogenic  leukaemia)  large  mononuclear  leukocytes  with 
neutrophile  granules  are  found  (myelocytes) .°  (See  Plate  I.,  Figs.  6 
and  7.) 

1  Green,  Pathology  and  Morbid  Anatomy.  2  ibid.  s  ibid. 

*  Cabot,  Boston  Medical  and  Surgical  Journal.  =  Ziegler,  General  Pathology. 


74 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


Pernicious  Anaemia.  This  is  a  comparatively  rare  but  generally 
fatal  tlisease,  characterized  chiefly  by  a  great  fall  in  the  number  of  red 
corpuscles,  those  remaining  being  altered  in  form  and  size  and  showing 
evidences  of  degeneration.  The  total  hremoglobin  is  reduced,  but  the 
relative  amount  may  be  increased.  Degeneration  is  shown  by  pecu- 
liarities of  staining.  Normal  red  corpuscles  (normoblasts),  nucleated 
red  corpuscles  (megaloblasts),  large  nucleated  red  corpuscles  (giganto- 
blasts),  microcjies,  and  poikilocytes  are  found.  The  blood  platelets 
and  leukocytes  are  somewhat  diminished.^  The  ox}"gen-carrying  power 
is  markedly  lessened  and  all  tissues  suffer  from  malnutrition.  The 
power  of  coagulation  of  the  blood  is  lessened.  Marked  fatty  degenera- 
tion of  the  heart  muscles  is  apt  to  occur." 

COAGULATION  OF  THE  BLOOD. 


The  blood  when  drawn  from  the  body  or  in  contact  with  a  wounded 
surface  or  injured  vessel  wall  undergoes  a  process  of  solidification 
called  coagulation.  This  is  due  to  the  splitting  up  of  the  fibrinogen 
ordinarily  in  solution  in  the  blood  into  a  globulin  and  fibrin.     The 

latter  takes  the  form  of  a  network  in  the 
open  spaces  of  which  the  corpuscles  are 
entangled  (Fig.  46).  The  formation  of 
fibrin  is  brought  about  by  the  activity  of 
an  unorganized  ferment  (fibrin  ferment  or 
thrombin)  liberated  by  injured  white  cor- 
puscles. For  the  production  of  this  fer- 
ment calcium  salts  are  necessary.^  Coagu- 
lation may  occur  in  the  living  vessel,  as  a 
thrombus,  or  in  the  interstitial  tissue,  as  in 

Fibrin  filiiments  and  blood  tab-      •     n  ,•  i   •     <>  ,• 

lets:  A.  network  of  fibrin,  shown    inflammation  and  infarction. 

after  washing  away  the  corpuscles  ThTOmbOSiS.       The  formatloU  of  thrOmbl 
from  a  prepaimtion  of  blood  that 

has  been  allowed  to  clot;  many  of  Or  clotS   "^dthiu  the    liviug  VCSScl    may   OCCUF 

the  filaments  radiate  from  small  -^   ^^^    ^^^^^    artericS,    VciuS,    Or    CapillaricS. 

If  the  blood  stream  be  somewhat  retarded 

an  increased  number  of  white  corpuscles 

and  blood  platelets  occupy  the  peripheral 

zone  and  adhere  to  the  vessel  wall.     If  the  vessel  wall  be  injured  the 

blood  platelets  become  attached  to  it.     With  these  platelets  the  white 


clumps  of  blood  tablets.  £  (from 
Osier),  blood  corpuscles  and  ele- 
mentary particles  or  blood  tablets 
within  a  small  vein. 


1  Green,  Pathologj-  and  Morbid  Anatomy. 
•*  Kirke's  Physiology. 


2  Ibid. 


COAGULATION  OF  THE  BLOOD. 


75 


corpuscles  and  sometimes  the  red  become  deposited.  Fibrin  forms 
and  the  corpuscles  are  included.  The  thrombus  is  red  when  red 
corpuscles  are  included  in  it;  white  when  only  white  corpuscles  are 
present.  The  causes  of  thrombosis  are  these:  1.  A  retardation  of 
the  blood  current  at  some  point  from  some  cause.     2.  Local  changes 


Fig.  47. 


A  thrombus  in  the  saphenous  vein,  showing 
the  projection  of  the  conical  end  of  the  throm- 
bus into  the  femoral  vessel :  S,  saphenous 
vein  ;  T,  thrombus ;  C,  conical  end  projecting 
into  femoral  vein.  At  i',  v,  opposite  the 
valves,  the  thrombus  is  softened.    ( Virchow. ) 

in  the  walls  of  the  vessels  and 
probably  pathological  changes  in 
the  blood.^ 

Older  thrombi  are  firmer  than 
those  recently  formed.  Thrombi 
are  also  formed  in  the  capillaries. 

Diagram     to     show    phenon.ena    of    venous  cirCUmstaUCC  which  faVOrS   the 

tlirombosis :  v,  v,  valves  of  veins ;  o,  o,  primary 

thrombus  (white);  e,  d,  e,/,sr,  secondary  white  spOUtaUCOUS   CCSSatioU  of    hcmor- 
thrombi  connected  with  primary  white  throm-                                                            „  .  , 

bus  by  various  reel  thrombi; /I,  piece  of  white    rhagc.     1  hcy  may  lorm   m   the 

thrombus  becoming  detached  by  blood  current,      ygggels      in      inflammation.  Rc- 

(Green,  modified  from  Thoma.) 

maining  in  the  situations  in  which 
they  were  formed,  they  either  undergo  simple  or  puriform  softening  or 
are  calcified  or  are  resorbed  and  replaced  by  connective  tissue.  (See 
Regeneration.)  The  calcified  varieties  are  called  phleboliths  in  the 
veins;  arterioliths  in  the  arteries.  In  senile  gangrene  a  thrombus 
may  extend  a  great  distance. 

Embolism.     Portions   of   the   softened   varieties   of   thrombi  may 
become  detached  and  float  about  in  the  blood;  these  are  called  emboli. 


'  Ziegler,  General  Pathology. 


76 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


Other  foreign  substances  may  act  as  emboli  —  c.  cj.,  air  or  fat- 
globules. 

If  the  thrombus  be  septic,  as  in  the  case  of  puriform  softening,  the 
emboli  may  lodge  in  small  vessels  and  cause  secondary  septic  disease 
processes,  as,  for  example,  in  the  cases  of  pyaemia  accompanied  by 
infarctions. 

Infarction.  "\Mien  an  embolus  occludes  a  terminal  artery,  that  is,  an 
artery  whose  branches  spread  like  those  of  a  tree  without  anastomosis, 
the  backward  pressure  from  the  vein  upon  the  blood  in  the  capillaries 
causes  an  extravasation  of  blood  into  the  interstitial  tissue  of  the 
wedge-shaped  area,  forming  what  is   called  a  hemorrhagic   infarct. 


Fig.  50. 


Embolus  impacted  at  the  bifurcation  of  a 
brancli  of  the  pulmonary  artery,  showing  the 
formation  of  thrombi  behind  and  in  front  of 
it,  and  the  extension  of  these  as  far  as  the 
entrance  of  the  next  collateral  vessels :  E, 
embolus ;  t,  t',  secondary  thrombi.   (Virchow. ) 


Diagram  of  a  hemorrhagic  infarct :  a,  artery 
obliterated  by  an  embolus  (e) ;  v,  vein  filled 
with  a  secondary  thrombus  (th) ;  1,  centre  of 
infarct  ■which  is  becoming  disintegrated;  2, 
area  of  extravasation;  3,  area  of  collateral 
hypersemia.     (O.Weber.) 


A  clot  forms,  degeneration  of  the  clot  occurs,  and  if  aseptic  it  is 
absorbed  and  replaced  by  connective  tissue  (see  Regeneration);  if 
caused  by  a  septic  embolus,  it  may  be  involved  in  the  resulting  septic 
process — e.  g.,  in  pysemic  metastatic  abscess.  Infarction  has  been 
held  by  Black  to  occur  in  the  dental  pulp.  No  demonstration  has, 
however,  been  made. 

Hemorrhagic  Diathesis.  This  is  a  condition,  largely  hereditary,  in 
which  coagulation  does  not  close  wounds  readily,  and  ordinarily  trivial 
wounds  may,  in  spite  of  surgical  aid,  induce  death  by  hemorrhage. 
Hereditary  hemorrhagic  diathesis  (haemophilia)  is  usually  transmitted 
through  the  female  line  to  the  male  line — i.  e.,  from  grandfather  to 
grandson  through  the  gi'andfather's  daughter — and  seven  or  more  gen- 


COAGULATION  OF  THE  BLOOD.  77 

erations  of  hsemophilics  have  been  recorded/  Males  suffer  more  than 
females  in  the  ratio  of  about  11  to  1. 

According  to  Legg,^  "It  is  of  three  degrees  of  severity: 

"  1.  Characterized  by  external  and  internal  bleedings  of  every  kind 
and  by  joint  affections. 

"  2.  By  spontaneous  hemorrhages  from  mucous  membranes,  but  no 
traumatic  bleeding  or  ecchymoses,  and  no  joint  affections. 

"  3.  A  tendency  simply  to  ecchymoses.  The  first  is  seen  most  fre- 
quently in  men,  the  second  in  women;  the  third  may  appear  in  either 
sex." 

The  joint  affections  are  due  to  hemorrhage  and  simulate  rheumatic 
affections.  Heemophilics  are  apt  to  be  thin-skinned,  neurasthenic, 
and  liable  to  sudden  flushings  and  vasomotor  disturbances.^  Blondes 
suffer  more  than  brunettes.* 

The  injured  part  may  bleed  from  the  first  or  a  normal  clot  may  form 
and  secondary  hemorrhage  or  capillary  oozing  occur.  Death  may 
rapidly  occur  or  the  patient  bleed  to  fainting  or  until  almost  dead  and 
hemorrhage  then  cease.  This  may  require  any  period,  even  weeks. 
The  pathology  of  the  condition  is  uncertain.  Fillebrown^  reports  a  fatal 
case  in  which  the  arteries  were  excessively  thin.  Porter  points  out  that 
the  blood  may  clot  in  the  receptacle,  yet  not  in  the  small  vessels  of  the 
wound,  and  infers  that  some  hereditary  deficiency  exists  which  inter- 
feres with  the  action  of  the  vasoconstrictors. 

Haemophilics  usually  manifest  a  history  of  bleeding  before  puberty, 
and  haemophilic  infants  have  died  from  hemorrhage  due  to  gum- 
lancing,  circumcision,  etc.  The  therapeutic  measures  indicated  are 
local  styptics,  compresses,  etc.  Haemostatics  internally,  dilute  sul- 
phuric acid,  hydrastis  canadensis,  calcium  chloride,  and  gelatin  locally 
and  by  injection.''  Absolute  quiet  and  the  withholding  of  food  for  two 
days;  the  hunger  to  be  relieved  by  small  doses  of  opium  and  thirst  by 
ice-water  in  small  quantities.^  The  acute  anaemia  induced  requires 
treatment. 

Individuals  known  to  be  haemophilic  should  live  a  hygienic  life  and 
avoid  all  injuries,  however  slight,  possible  to  avoid.  If  operation  be 
unavoidable  they  should  be  treated  with  calcium  chloride,  gr.  iij  ter 
die,  for  not  more  than  four  days,  as  thereafter  the  coagulability  of  the 
blood  is  decreased.^ 

1  Porter,  InternatioBal  Dental  Journal,  1900.  -  Musser,  Medical  Diagnosis. 

3  Porter,  loc.  cit.  4  Thompson,  Practical  Medicine. 

5  International  Dental  Journal,  1900.  6  Hare,  Practical  Therapeutics. 

^  Porter,  loc.  cit.  8  Hare,  loc.  cit. 


78  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

LOCAL   DISTURBANCES  OF   THE   CIRCULATION. 

The  amount  of  blood  in  a  part  may  be  increased  or  diminished. 
The  types  of  local  disturbance  of  the  circulation  differ  as  to  causes, 
phenomena,  and  effect,  and  as  to  the  indicated  treatment  for  each. 

In  health  the  bloodvessels  are  maintained  at  a  proper  calibre  through 
the  action  of  two  sets  of  vasomotor  nerve  fibres: 

1.  The  vasoconstrictors,  which  control  the  involuntary  muscles  of 
the  vessel  wall  and  which,  when  stimulated,  cause  contraction  of  the 
vessel. 

2.  The  vasodilators,  which,  when  stimulated,  inhil^it  the  muscular 
action  and  permit  dilatation. 

Arterial  Hyperaemia.  Arterial  or  active  hyperemia  is  a  more  or 
less  prolonged  increase  in  the  amount  of  blood  in  the  dilated  arteries 
of  a  part.  It  expresses  the  reaction  which  occurs  as  the  consequence 
of  the  presence  of  an  irritant,  the  action  of  which  lessens  the  arterial 
tension  and  permits  dilatation  with  a  consequent  excess  of  blood. 

Causes.  The  lessened  arterial  resistance  is  produced  either  by  a 
stimulation  of  the  vasodilator  nerves  or  a  sedation  or  paralysis  of  the 
vasoconstrictor  nerves.  Certain  causes  act  to  produce  constriction  of 
the  vessels,  but  later  the  muscle  cells  of  the  walls  are  fatigued  and 
dilatation  results — e.  g.,  the  reaction  after  the  prolonged  application 
of  cold. 

The  removal  or  diminution  of  pressure,  to  which  vessels  have  become 
accustomed,  is  also  a  cause  of  their  dilatation;  often  sudden  enough 
to  cause  bursting. 

Irritants  and  mild  injuries  act  upon  the  sensory  nerves  of  a  part,  and 
by  reflex  action  through  the  vasomotors  (sympathetic  system)  produce 
hyperaemia  of  the  part  itself — e.  g.,  heat. 

Irritation  of  sensory  nerves  may  induce  a  reflex  hyperemia  in  other 
parts  to  which  branches  of  the  same  nerve  are  distributed — e.g.,  the 
peripheral  hyperaemia  of  neuralgia,  induced  by  irritation  of  a  tooth 
pulp. 

A  similar  effect  may  be  produced  in  deep-seated  organs  to  which 
other  nerves  are  distributed — e.  g.,  hyperaemia  of  deep  organs  through 
the  application  of  irritants  to  the  skin  over  them  or  hyperaemia  of  the 
intestinal  wall  (tenth  nerve)  as  the  result  of  the  stimulation  of  a  pulp 
underlying  an  erupting  tooth  (fifth  nerve). 

Collateral  hyperaemia  is  induced  by  the  diminished  flow  of  blood  to 
other  parts — e.  g.,  by  the  bandaging  of  parts  or  through  the  chilling  of 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION.  79 

the  surface  of  the  body.  A  part  having  a  lessened  resistance  may 
become  hypercemic. 

Compensatory  hyperaemia  may  occur  through  the  removal  of  one  of 
a  pair  of  organs;  the  other  receives  the  excess  of  blood,  sometimes 
becomes  hypertrophied,  and  takes  upon  itself  an  increased  amount 
of  work.     (See  Hypertrophy.) 

Arterial  hypersemia  is  produced  as  the  first  step  in  the  process  of 
inflammation.     (See  Inflammation.) 

Pathology.  The  arteries  are  dilated;  there  is  an  increased  flow  of 
blood  through  them  and  also  to  them  through  their  own  nutritive 
arteries;  the  pressure  in  the  veins  rises  as  the  veins  are  enlarged  to 
accommodate  the  blood.  As  exudation  sometimes  does  not  increase 
markedly,  the  lymph  pressure  is  not  increased  except  in  marked  cases, 
in  which  some  oedema  may  occur.  The  function  of  the  part  may  be 
disturbed  in  the  more  marked  cases.  (For  illustrations,  see  Chapter 
XVIII.) 

Results.  Continued  arterial  hypersemia,  as  a  rule,  results  in  an 
increase  of  nutrition.  The  arteries  may  be  permanently  enlarged,  their 
walls  thickened,  and  the  tissues  about  them  hypertrophied  in  con- 
sequence of  the  increased  capacity  for  work  in  the  part.  Hyperses- 
thesia  of  nerves  and  nervous  tissue  is  often  a  result.  In  marked 
hyperaemia  with  function  altered  there  is  a  tendency  to  the  degener- 
ations.   (See  Arterial  Hyperaemia  of  the  Pulp.) 

Symptoms.  These  naturally  would  be  and  are  increased  redness, 
temperature,  and  sensibility;  more  or  less  throbbing,  in  some  cases 
swelling  and  throbbing  pain.  The  increased  temperature  is  due  to 
the  increased  oxidation. 

Degrees  of  Hyperaemia,  It  is  to  be  borne  in  mind  that  the  hyper- 
aemia may  be  of  several  grades,  varying  from  a  very  mild  exaltation  of 
function  and  sensation  to  a  distinctly  pathological  condition  with 
altered  function.  The  effects  may  be  constructive  in  character  or 
destructive,  the  former  due  to  the  increased  nutrition,  the  latter  to 
interference  with  it.  (See  Constructive  and  Destructive  Diseases  of 
the  Pulp.) 

Hyperaemia  as  a  Local  Predisposition.  It  is  generally  acknowledged 
that  the  presence  of  a  local  hyperaemia  lessens  the  resistance  of  a  part 
to  the  action  of  pathogenic  bacteria — e.  g.,  hyperaemia  of  the  lungs 
to  diplococcus  pneumoniae. 

Treatment.  The  principle  underlying  the  treatment  is  to  remove 
the  cause  and  procure  surgical  rest.    The  symptoms,  as  a  rule,  then  sub- 


80  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

side  promptly.  It  may  be  that  the  conditions  require  treatment  irre- 
spective of  the  cause,  which  may  not  be  determined  or  be  absent,  the 
vessels  being  dilated  as  the  effect  of  a  previously  acting  cause.  The 
effect  aimed  at  is  the  reduction  of  the  dilated  vessels.  This  is  attempted 
at  times  through  the  use  of  drugs;  for  example,  ergot  stimulates  the  vaso- 
constrictor system  and  lessens  the  calibre  of  all  the  vessels,  including 
those  affected.  The  antagonist  of  ergot,  aconite,  reduces  the  heart 
action  by  paralyzing  the  motor  apparatus  of  the  heart,  thus  reduc- 
ing the  arterial  pressure.^  Less  blood  is  delivered  to  a  part  in  a  given 
time.  Many  cases  of  superficially  seated  hyperemia  are  amenable  to 
local  treatment. 

Local  sedation  of  sensory  nerves  and  contraction  of  vessels  are  pro- 
duced by  application  of  dry  or  wet  cold  (ice-bags,  ice  wrapped  in 
muslin,  cloths  taken  in  succession  from  a  block  of  ice,  etc.) ;  also  by  the 
application  of  sedative  astringents,  as  the  liquor  plumbi  subacetatis 
in  the  well-known  formula  of  lead-water  and  laudanum — 

9; — Tinctuvie  opii,  f  jj ; 

Liq.  plumbi  subacetatis,  fSj ;     ■ 

Aquae,  Oj — M. ; 

in  which  to  the  astringent  effect  of  the  lead  is  added  the  sedative  effect 
of  the  opium. 

The  principle  of  derivation  is  also  employed.  What  is  known  as 
counterirritation  is  a  common  means  of  treatment.  An  irritant  such 
as  a  mustard  plaster  or  a  blister  or  dry  cup  applied  at  a  distance  to  the 
affected  part  induces  a  flow  of  blood  to  the  point  of  application  and 
lessens  the  amount  of  blood  in  the  area  of  hypersemia.  The  volume 
of  the  blood  being  in  definite  amount,  if  an  excess  exist  in  any  part  a 
deficiency  will  be  found  in  other  parts. 

The  hot  pediluvium  acts  upon  this  principle  by  drawing  a  consider- 
able excess  of  blood  into  the  vessels  of  the  lower  extremities.  This 
action  is  increased  by  adding  a  small  quantity  (two  or  three  tablespoon- 
fuls)  of  mustard  to  the  hot  water.  It  is  suggested  by  Endelman  that 
the  water  be  at  first  only  warm  and  the  hot  water  added  as  the  vessels 
relax.^ 

The  volume  of  the  blood  may  be  actually  reduced  and  a  derivative 
hyperaemia  of  the  sweat  glands  be  produced  by  the  use  of  diaphoretics. 
Cathartics  lessen  the  blood  volume  and  cause  mild  hyperaemia  of  the 
alimentary  canal.     Diuretics  act  in  a  similar  way  upon  the  kidneys. 

1  Biddle,  Materia  Medica  and  Therapeutics. 
-  Dental  Cosmos,  1904. 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION. 


81 


<_.^ 


In  deep-seated  hypersemia  counterirritation  is  valuable  alone  or  con- 
joined with  other  forms  of  derivation. 

Venous  Hypersemia.  Venous  (mechanical  or  passive)  hypersemia 
is  an  excess  of  blood  in  a  part  beginning  in  the  veins,  which  are 
dilated. 

Causes.  1.  Any  mechanical  interference  with  the  passage  of  the 
blood  through  the  veins  on  its  way  to  the  heart — e.  g.,  the  action  of 
bandages,  tumors  pressing  on  veins,  thrombi  in  veins,  etc. 

2.  Insufficiency  of  any  of  the  mechanical  forces  aiding  the  propulsion 
of  the  blood  through  the  veins — e.g.,  diminished  cardiac  power  or 
valvular  insufficiency,  obstructions, 
dilatations,  or  rigidity  of  arteries; 
insufficient  muscular  contraction 
upon  or  valvular  incompetency  in 
veins,  or  lessened  or  excessive  tho- 
racic aspiration,  etc.  The  second 
class  of  causes  produces  a  collection 
of  blood  in  the  veins  and  a  conse- 
quent reduction  of  volume  in  the 
arterial  system. 

Pathology.  The  veins  are  dilat- 
ed, the  current  is  slowed,  and  the 
intravenous  pressure  is  increased, 
in  consequence  of  which  watery 
(serous)  exudations  occur  in  the  parts  about  them  (oedema).  For  the 
same  reason  in  marked  cases  diapedesis  of  red  corpuscles  may  occur, 
and  their  haemoglobin  may  be  dissolved  out.  The  blood  in  the  parts 
not  being  sufficiently  changed,  and  in  some  cases  in  a  state  of  stasis, 
there  is  a  lessened  food  supply  and  waste  removal,  and  cell  nutrition 
suffers  accordingly.  Vital  processes  are  lessened,  secretion  is  dimin- 
ished, there  is  less  oxidation,  and  hence  less  heat  is  produced  and  less 
work  is  done.  Degeneration,  atrophy,  and  in  markedly  continued  cases 
necrosis  may  occur.  Long-continued  venous  hypereemia  with  great 
intravenous  pressure  may  produce  dropsies.  The  exudate  of  venous 
hypersemia  differs  markedly  from  that  of  inflammation.^ 


Venous  hypersemia  of  the  liver.  Two 
capillaries  near  central  hepatic  vein.  Show- 
ing the  thickening-  of  the  walls  and  the  accu- 
mulation of  red  blood  corpuscles  within 
them.     X  500.      (Green.) 


Hyperxmic  Exudate. 

Ivflammatory  Exudate. 

Poor  in  albumin. 

Eich  in  albumin. 

Rarely  coagulates  in  the  tissue. 

Usually  coagulates  in  the  tissue. 

Contains  few  cells. 

Contains  numerous  cells. 

Low  specific  gravity. 

High  specific  gravity. 

Contains  no  peptone. 

Contains  peptone  (product  of  cell  disintegration' 

1  Park's  Surgery. 
6 

82  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

Treatment.  Tlie  treatment  consists  of  the  removal  of  the  mechanical 
obstruction  to  the  return  of  the  blood  and  mechanical  support  of  the 
engorged  vessels,  with  a  view  to  recovery  of  the  tone  of  their  muscular 
walls.  This  latter  is  atcomplished  by  means  of  elastic  bandages  or 
compresses,  and  in  situations  in  which  these  cannot  be  used  astringents 
may  be  employed.  The  part  is  elevated,  when  possible,  to  aid  in  the 
return  of  the  blood  to  the  heart.  In  certain  circumstances,  as  in  an 
engorged  tooth  pulp,  actual  depletion  of  the  engorged  part  must  be 
resorted  to  by  blood-letting.     (See  Destructive  Diseases  of  the  Pulp.) 


INFLAMMATION. 

Inflammation  may  be  defined  as  a  series  of  hypergemic  changes 
expressive  of  the  reaction  of  living  tissue  against  an  irritant,  and  char- 
acterized chiefly  by  an  excessive  diapedesis  of  white  corpuscles  and 
exudation  of  coagualable  lymph  from  the  bloodvessels. 

Causes.  Any  irritant  or  injury  capable  of  producing  a  lesion  of  the 
bloodvessel  wall  not  involving  its  immediate  death  can  produce  inflam- 
mation. In  case  direct  death  is  produced  the  inflammation,  if  any, 
occurs  in  the  tissue  contiguous  to  the  dead  part. 

The  causes  of  inflammation  may  be  divided  first  into  non-septic 
and  septic  or  infective.  The  non-septic  causes  may  be  extrinsic  or 
intrinsic.  The  extrinsic  non-septic  causes  are:  1.  Physical  irritants, 
such  as  violence,  mechanical  irritation,  pressure  or  traumatism,  exces- 
sive heat  or  cold,  and  electrolytic  action.  2.  Chemical  irritants — e.  g., 
the  action  of  acids,  caustics,  etc.  3.  Nervous  or  vital  irritants — 
e.g.,  rubefacients,  epispastics,  arsenic,  etc.  These  act  only  on  living 
tissue  through  the  medium  of  the  nerves. 

An  intrinsic  non-septic  cause  may  produce  inflammation — e.  g., 
urates  in  tissue,  mechanical  strains  upon  tissue,  temporary  lack  of 
blood  in  a  vessel  or  central  nervous  disturbance,  as  in  herpes  from 
locomotor  ataxia. 

Non-septic  causes,  as  a  rule,  produce  only  such  mild  inflammatory 
phenomena  as  are  concerned  in  circumvallation  of  an  irritant,  absorp- 
tion of  it,  and  in  repair  or  production  of  new  tissue.  No  pus  is  pro- 
duced unless  pyogenic  bacteria  gain  ingress.  This  class  of  inflamma- 
tion is  termed  simple  inflammation. 

Septic  or  Infective  Causes.  These  are  fungi  or  their  products, 
and  the  classes  of  inflammations  produced  are  much  more  severe,  con- 


INFLAMMATION. 


83 


tinuous,  and  destructive  in  their  nature,  and  are  termed  infective  inflam- 
mations. 

Pathology  of  Simple  Inflammation.  If  to  the  web  of  a  frog's  foot 
tincture  of  capsicum  be  appUed  or  if  its  mesentery  be  exposed  to  the 
air  and  either  be  examined  under  the  microscope  while  the  animal  is 
living,  it  is  noted  that  after  a  possible  short  period  of  contraction  of  the 
arterioles  dilatation  of  arteries  at  once  begins  and  is  gradually  followed 
by  dilatation  of  the  veins  and  capillaries.  This  continues  to  steadily 
increase  for  about  twelve  hours.  During  the  first  hour  of  this  period 
the  blood  current  is  accelerated  and  arterial  hyperemia  may  thus  be 


Fig.  52. 


Small  vein  in  mesentery  of  dog,  after  exposure  for  half  an  hour  and  irrigation  with  salt 
solution :  a,  red  corpuscles ;  6,  leukocytes  adhering  to  wall  of  vein ;  e,  red  corpuscles ;  d 
leukocytes  which  have  escaped  from  vessel;  e,  leukocyte  in  act  of  escaping;  /,  fibrous  tissue. 
X  340.     Modified  from  Thoma.     (Green.) 

said  to  be  the  first  stage  of  an  inflammation.  Following  this  accelera- 
tion the  blood  flow  is  increasingly  retarded.  The  retardation  is  due  to 
the  action  of  the  leukocytes,  large  numbers  of  the  mononuclear  and 
polymorphonuclear  forms  of  which  fall  out  of  the  central  blood  stream 
into  the  periaxial  stream  and  collect  along  the  walls  of  the  small  veins 
(Fig.  52,  6).  Several  layers  of  leukocytes  may  thus  form.  Probably 
some  peculiar  attraction  exists  between  the  leukocytes  and  the  wall  of 
the  vessel. 

This  massing  of  leukocytes  compels  the  red  corpuscles  to  the  centre 
of  the  stream  (Fig.  52,  a)  and  their  passage  is  mechanically  interfered 
with,  and  the  further  dilatation  of  the  vessel  becomes  a  process  of 


84  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

venous  hypei'Eemia.     The  vessels  are  increased  in  size  and  length  and 
become  more  tortuous.    Pulsation  is  noted. 

Coincident  with  retardation  of  the  blood  flow,  the  leukocytes  are  seen 
to  work  their  way  by  an  amoeboid  movement  through  the  stomata  of 
the  veins  and  to  some  extent  of  the  capillaries  into  the  perivascular 
spaces — i.  e.,  into  the  adjoining  tissue — in  which  they  may  move  far 
from  their  point  of  escape  and  mass  about  the  irritant  if  one  be  present. 
This  process  is  called  diapedesis  (Fig.  52,  e).  At  the  same  time  a  fluid 
rich  in  albumin,  and  thus  capable  of  coagulation,  escapes  by  the 
same  route  into  the  tissue  (Fig.  53). 

As  the  venous  hypereemia  increases  the  flow  of  red  corpuscles  in  the 
veins  is  increasingly  retarded  until  stopped,  when  a  to-and-fro  motion 
(oscillation)  begins.    Some  red  corpuscles  may  escape  into  the  tissue. 

Finally  all  motion  ceases,  diapedesis  ceases, 
^J^i^  ^  and  stasis  is  complete.     This  blood  may 

"^^57-   ,--^    ^..        -\       remain  fluid  in  the  vessel  for  several  days 
~  ;^        (i.  e.,  without  coagulation),  and  if  the  blood 

:^-  flow  be  re-established  the  separate  red  cor- 
puscles are  seen  one  by  one  to  roll  away 
from  the  general  mass  until  all  are  in  move- 
ment and  stasis  ceases  (Thoma). 

Inflammatory  oedema  of  skin.  .  ,  ,  i        •   \  i 

The  large  spaces  shown  were        Coagulatiou  (thrombosis)  may,  howcvcr, 
filled  with  exuded  fluid.    X  2>^.    ^^^^j.  -^^  ^^le  vcsscls  iuvolvcd  in  the  stasis 

(Boyd.) 

and  the  part  be  later  removed  through  the 
process  of  resorption.  (See  Resorption  of  Clot.)  With  the  inflam- 
mation fully  established  there  are  in  the  tissue  the  following  abnormal 
elements : 

1.  Leukocytes  and  some  red  corpuscles.  2.  Coagulable  lymph.  3. 
Later  new  embryonic  cells  which  surround  the  leukocytes  massed  about 
the  irritant.  These  are  fibroblasts  ready  to  form  scar  tissue — i.  e.,  they 
are  the  elements  composing  granulation  tissue. 

The  disposition  of  these  elements  of  inflammation  is  as  follows: 
The  leukocytes  mass  about  the  irritant,  exert  a  certain  amount  of 
phagocytic  activity,  and  may  in  turn  be  injured,  liberating  fibrin 
ferment,  which,  acting  upon  the  fibrinogen  of  the  lymph,  produces 
fibrin,  which  in  turn  forms  a  coagulum.  This  coagulum  blocks  the 
lymphatic  vessels  leading  from  the  part  involved,  thus  causing  a 
retention  of  fluid  in  the  tissue. 

In  the  later  stages  of  non-infective  inflammation  the  tissue  cells 
undergo  multiplication,  forming  cells  larger  and  having  more  power 


INFLAMMATION. 


85 


of  amoeboid  movement  and  phagocytosis  than  the  leukocytes.  These 
become  mingled  with  the  leukocytes  in  the  area  of  inflammation.  They 
are  fibroblasts  from  which  all  the  connective  tissues  develop,  and  to 
the  action  of  which  regeneration  is  mainly  due.  Around  and  about  the 
focus  of  inflammation  the  bloodvessels  are  in  a  condition  of  arterial 
hypersemia  and  about  this  is  an  area  of  normal  tissue.  These  areas 
shade  off  into  each  other.  The  phagocytes  cause  dissolution  of  coagula 
and  dead  aseptic  tissue^  and  remove  them.  If  the  irritant  be  thus 
removable,  it  is  eaten  away.    If  the  dead  tissue  be  superficial,  the  con- 


Acute  bronchial  catarrh :  passage  of  leukocytes  through  the  epithelium  of  the  bronchus  between 
the  ciliated  cells.     X  700.     (Thoma.) 

nection  with  the  living  tissue  beneath  is  eaten  through  and  the  latter 
thrown  off.  If  the  superficial  tissue  have  been  previously  removed,  the 
wound  is  covered  with  the  exudates  and  leukocytes,  which  dry  into  a 
scab,  beneath  which  regeneration  occurs.  If  inflammation  occur  in  a 
mucous  surface,  the  exudate  and  corpuscles  escape  from  the  sub- 
mucous tissue  between  the  epithelial  cells  as  a  catarrhal  discharge 
(Fig.  54) .  If  the  inflammatory  exudate  be  highly  coagulable  and  coagu- 
late, firm  swelling  is  caused,  apt  to  lead  to  organization  of  tissue, 
hence  called  fibrinous  inflammation.    If  it  be  productive  of  hypertrophy. 


86  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

it  is  called  productive  inflammation.  If  the  exudate  be  watery,  poor 
in  albumin,  and  hence  not  readily  coagulable,  the  inflammation  is 
called  serous  inflammation. 

Symptoms  of  Simple  Inflammation.     These  are: 

1.  Redness  due  to  the  excess  of  blood  in  the  vessels  and  in  the  tissue. 
In  some  cases  the  part  may  have  a  dusky  hue.  The  color  is  deepest 
in  the  area  of  greatest  stasis. 

2.  Heat  due  to  the  increased  oxidation  in  the  area  of  hypersemia 
about  the  area  of  stasis.  It  has  been  shown  that  there  is  no  increased 
heat  in  the  area  of  stasis.    In  this  area  chemical  action  is  lessened. 

3.  Swelling  due  to  the  excess  of  blood  in  the  vessels,  the  exudates  of 
leukocytes  and  fluid,  and  the  multiplication  of  tissue  cells.  The  hard- 
ness of  a  swelling  is  due  to  coagulation  of  the  fluid  exudate. 

4.  Pain;  the  result  of  the  pressure  of  the  effusion  upon  sensory  nerve 
terminals;  it  is  frequently  throbbing  in  correspondence  with  the  heart 
beat;  the  impulse  causes  temporarily  increased  pressure  upon  the  nerve 
terminals.  Gravitation  also  increases  the  pressure  and  pain  in  a 
dependent  part — e.  g.,m  a  hand  or  foot  or  in  recumbency  in  case  of 
pulpitis  (which  see). 

5.  Impaired  junction  is  an  evident  result  of  a  disturbance  involving 
such  pathological  phenomena  as  have  been  described. 

There  are  no  general  disturbances  in  simple  inflammation  beyond  a 
slight  traumatic  fever  due  to  absorption  of  some  aseptic  material  from 
the  seat  of  inflammation — e.  g.,  fibrin  ferment.^ 

Infective  Inflammation.  If  micro-organisms  enter  the  tissue  through 
a  wound  or  puncture  or  an  abraded  surface,  or  if  they  locate  upon 
predisposed  or  non-resistant  mucous  membrane,  their  multiplication 
causes  irritation  and  inflammation  of  the  tissue  about  them.  This  at 
first  resembles  a  simple  inflammation,  but  later  becomes  more  severe, 
prolonged,  and  may  spread  into  the  surrounding  tissue,  or  in  some 
cases  cause  inflammation  in  another  place  in  no  way  connected  with 
it  except  by  the  blood  or  lymphatic  channels  (metastasis).  Briefly, 
the  process  may  be  described  as  beginning  with  the  entrance  or  location 
of  the  organisms  and  their  multiplication.  An  injury  of  the  vessel  walls 
occurs  and  the  phenomena,  such  as  occur  in  simple  inflammation, 
begin.  There  is  arterial  hypersemia,  later  retardation  of  the  blood 
current;  diapedesis  of  leukocytes  occurs,  and  a  copious  exudate  of 
coagulable  lymph  is  poured  out  into  the  intervascular  tissue.  By  posi- 
tive chemotaxis  the  leukocytes  are  attracted  to  the  bacteria,  surround 

1  Green's  Pathology  and  Morbid  Anatomy. 


INFLAMMATION.  87 

them,  and  apparently  endeavor  to  limit  their  activity,  or,  perhaps,  to 
digest  them.  If  the  bacteria  be  few  in  number  and  not  too  virulent,  the 
phagocytes  are  successful  and  the  phenomena  of  resolution  occur.  If, 
however,  the  contrary  be  the  case,  the  leukocytes  are  overcome  and  the 
inflammation  spreads.  The  central  or  most  involved  area  dies.  It  is 
thus  seen  that  there  may  be  two  terminations  of  an  infective  inflam- 
mation, resolution  and  necrosis. 

Resolution.  If  the  phagocytes  destroy  or  wall  up  the  bacteria,  so 
that  they  die  in  their  own  products  or  are  killed  by  the  protective  juices 
of  the  part  (alexins),  the  lymphatics  are  unblocked,  the  circulation  is 
re-established,  the  tissue  that  has  died  is  removed  by  resorption  and 
replaced  by  scar  tissue  if  the  loss  be  considerable.  No  evident  pus  nor 
externally  evident  necrosis  is  produced,  and  the  part  exhibits  phe- 
nomena much  like  those  of  a  simple  inflammation.  This  is  the  only 
termination  for  a  simple  (non-infective)  inflammation. 

Necrosis.  Death  of  a  part  may  result  from  infective  inflammation, 
either  with  or  without  pus  formation. 

Suppuration.  If  the  irritant  in  the  tissue  consist  of  pyogenic 
organisms,  such  as  the  staphylococcus  pyogenes  aureus  or  albus,  the 
streptococcus  pyogenes,  the  bacillus  pyocyaneus,  bacillus  typhi  abdomi- 
nalis,  diplococcus  pneumonise,  or  the  gonococcus,  pus  will  be  formed, 
provided  the  germs  be  not  killed  out.  The  staphylococcus  pyogenes 
aureus  is  most  frequently  the  organism  infecting  wounds.  It  is  prac- 
tically universal. 

Entering  a  part  the  bacteria  distributed  in  the  tissue  act  as  irritants 
and  excite  the  phenomena  of  inflammation  as  described.  Some  of  the 
cocci  are  taken  up  by  the  fixed  connective-tissue  corpuscles,  the  leuko- 
cytes, and  the  endothelial  cells  of  the  capillaries,  and  some  lie  free  in 
the  tissue.  The  cocci  multiply  and  the  polymorphonuclear  and  eosino- 
phile  leukocytes  increase  in  number  by  diapedesis  and  surround  them. 
The  original  tissue  cells,  including  those  of  the  bloodvessels,  undergo 
coagulation  necrosis  as  the  result  of  the  action  of  bacterial  ferments  and 
do  not  take  up  staining  reagents  (Fig.  55).  Coagulation  of  the  exudates 
occurs.  The  leukocytes  and  tissue  cells  are  in  part  degenerated  into 
pus  corpuscles  by  the  action  of  the  unorganized  ferments  of  the  bac- 
teria— i.  e.,  their  nuclei  are  fragmented  and  they  undergo  fatty 
degeneration.  Some  cocci  die.  The  exudate  is  peptonized  into  a  fluid 
which,  together  with  the  cocci,  dead  leukocytes,  and  tissue  remnants, 
constitutes  -pus.  About  this  pus  is  a  circumvallating  wall  of  living 
leukocytes,  and  about  this  again  a  zone  of  fibroblasts  arranged  about 


88 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


new  capillary  loops  (granulation  tissue).    The  whole  constitutes,  when 
confined  within  tissue,  an  abscess.    When  upon  a  surface  the  granu- 


FlG.  55. 


6— 


:S:; 


Miliai-j'  abscess  in  a  case  of  septic  embolism  of  the  kidney  :  a,  leukocytes  advancing  towai'd 
and  surrounding  6,  a  mass  of  cocci,  in  whose  neighborhood  all  trace  of  structure  has  disap- 
peared; c,  renal  epithelium  too  damaged  by  bacterial  products  to  take  the  stain;  d,  kidney 
tissue  staining  normally;  e,  vein  from  which  leukocytes  are  making  their  way  to  the  com- 
mencing abscess.     X  100.     (Green.) 


lation  tissue  is  upon  the  under  side  only,  and  the  whole  constitutes  a 
suppurating  ulcer. 
While  the  leukoc}i;es  may  overcome  the  bacteria,  the  reverse  is  often 


INF  LAMM  A  TION.  8  9 

the  case,  and  the  pus  cavity  enlarges  in  the  same  manner  as  at  first  by 
a  new  formation  of  coagulation  necrosis,  more  circumvallation,  further 
liquefaction  of  the  coagulum,  etc.  The  path  offering  the  least  vital 
or  mechanical  resistance  is  usually  followed  until  the  surface  of  the 
body  or  some  internal  cavity  is  reached.  The  last  portion  of  tissue 
overlying  the  forming  pus  is  tumefied  and  a  soft,  yellow  spot  appears. 
This  is  called  pointing.  The  tissue  is  ruptured  by  the  internal  pressure 
and  the  pus  escapes.  The  tract  from  the  point  to  the  abscess  cavity 
is  a  fistula.  As  soon  as  this  occurs  granulation  tissue  springs  up  upon 
the  sides  of  the  abscess  cavity  and  usually  soon  fills  it  with  scar  tissue. 
(See  Regeneration.)  If  the  cause  continue  to  act,  as,  for  example,  in 
case  of  a  portion  of  dead  and  septic  bone  beneath  soft  tissue,  a  gan- 
grenous pulp  in  a  tooth  root  or  infected  crypts  of  the  abscess  walls,  the 


An  abscess  in  the  skin.  The  horny  layer  has  largely  disappeared,  and  the  Malpighian  layer 
is  pushed  upward  by  the  subjacent  abscess  (a).  The  mass  of  pus  corpuscles  is  just  breaking 
down  to  form  a  cavity,  the  walls  of  which  are  thickly  infiltrated  with  similar  cells.     (Boyd.) 

granulation  tissue  breaks  down  and  the  condition  is  one  of  ulceration  or 
a  chronic  abscess  with  a  fistula.  If,  in  the  course  of  abscess  formation, 
bone  be  encountered  by  the  pus,  it  may  be  and  often  is  molecularly 
broken  down  into  pus.  (See  Acute  Apical  Abscess.)  It  does  not  always 
happen  that  the  pus  finds  escape  either  naturally  or  through  surgical 
aid :  the  patient  may  die  before  this  occurs,  or  the  tissues  around  the 
seat  of  pus  formation  may  form  a  boundary  wall  which  the  organ- 
isms fail  to  break  down  and  thus  die  starved  out.  The  abscess  con- 
tents undergo  changes  resulting  in  caseation,  or  later  the  mass  may 
calcify.  (See  p.  64. )  The  streptococci  pyogenes  may  multiply  laterally, 
following  the  subcutaneous  cellular  tissue,  and  produce  violent  spread- 
ing inflammation  with  but  little  pus  formation — e.  g.,  some  forms  of 
apical  abscess  and  erysipelas. 


90  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

The  products  (toxins)  from  an  abscess  or  infective  inflammation 
may  find  their  way  into  the  blood  and  a  general  toxaemia  result,  or  the 
organisms  themselves  may  enter  the  blood  and  a  general  infection 
result  (septicaemia). 

There  are  various  varieties  of  pus  which  have  names  describing  the 
chief  characteristics: 

Creamy  pus  is  the  erroneously  called  laudable  pus  associated  with 
an  acute  abscess  or  ulcer  which  progresses,  as  a  rule,  toward  a  cure. 
It  is  of  a  yellowish-white  color,  creamy  consistency,  and  without  odor. 

Curdy  pus  contains  flakes. 

Ichorous  pus  is  thin,  odorous,  and  irritating. 

Muco-pus  is  pus  containing  mucus. 

Sero-pus  is  pus  containing  much  serum. 

Sanious  pus  contains  blood. 

Cause.  The  cause  of  suppuration  is  the  development  in  tissues  of 
pyogenic  organisms.  The  action  of  these  causes  is  favored  by  the 
presence  in  the  part  of  a  hypersemia  or  simple  inflammation,  such  as 
the  injury  introducing  the  organisms  may  cause.  These  as  well  as 
depraved  or  debilitated  tissues  favor  the  action  of  bacteria — i.  e.,  act 
as  predispositions. 

Symptoms.  The  symptoms  of  suppuration  are  both  general  and 
local. 

Local  Symptoms.  The  symptoms  of  inflammation  occur,  but 
usually  much  aggravated.  The  pain  is  often  of  a  lancinating  char- 
acter, sudden  darts  often  following  comparative  quiescence.  On  the 
other  hand,  the  throbbing  pain  may  be  continuous  and  intense,  espe- 
cially when  the  pus  is  confined  by  bone  or  tense  tissues,  as  in  case  of  a 
felon  or  acute  apical  abscess.  Recalling  that  around  the  pus  area  there 
is  one  of  active  inflammation,  and  about  that  hypersemic,  then  normal 
tissue,  one  may  judge  of  the  degree  of  involvement  of  deeper  parts  by 
the  appearance  of  the  surface  above  them.  Thus,  for  example,  hyper- 
aemia  at  the  surface  indicates  inflammatory  action  directly  beneath, 
while  inflammation  at  the  surface,  together  with  hardness  and  tume- 
faction, shows  a  more  involved  condition  of  the  tissue  directly  beneath 
it — i.  e.,  a  more  advanced  state  of  inflammation  or  even  of  suppuration. 

The  softening  of  the  apex  of  the  swelling  gives  a  feeling  of  lessened 
resistance,  indicating  pointing  or  pus  at  the  surface.  In  large,  super- 
ficial abscesses  the  sensation  known  as  fluctuation  may  be  obtained  by 
placing  one  finger  on  one  side  of  the  swelling  and  gently  tapping  upon 
the  other.     Yellowness  of  the  apex,  together  with  softness,  indicates 


INFLAMMATION. 


91 


that  the  abscess  is  about  to  discharge  its  contents.  A  fistula  upon  the 
surface  is  indicative  of  a  discharged  abscess,  and  leads  to  a  pus-forming 
area  beneath  (chronic  abscess). 

General  Symptoms.  If  toxsemia  be  produced,  there  may  be  chills, 
and,  at  the  same  time,  fever  as  high  as  104°  F.  A  full,  bounding  pulse 
accompanies  this,  and  there  are  other  evidences  of  septic  intoxication, 
which  may  become  profound.     (See  Septic  Intoxication.) 

Leukocytosis  after  surgical  disease  is  considered  pathognomonic  of 
suppuration. 

Ulceration.  The  development  of  micro-organisms  upon  a  free 
surface  causes  tissue  degeneration  and  death,  as  described  under 
abscess;  in  fact,  an  abscess  is  a  confined  ulcer. 

Numerous  forms  of  pathogenic  organisms  are  capable  of  causing 
tissue  degeneration  and  death  of  a  mucous  or  skin  surface.    If  infection 


Fig.  57. 


Tubercular  ulcer  of  the  intestine :  a,  mucosa;  b,  submucosa;  c,  musculai'is  ;  g,  ulcer; 
t,  tubercle  in  the  mucosa;  i',  focus  caseating  in  the  iniddle.     X  12. 

take  place  through  a  hair  follicle,  or  if  organisms  develop  upon  an 
abrasion,  or  in  the  epithelium  in  conditions  of  general  or  local  debility, 
the  epithelium  is  destroyed  over  an  area,  and  in  the  subepithelial  tissues 
the  organisms  multiply  and  cause  tissue  loss.  If  the  organisms  be 
pyogenic — and  ulcerous  surfaces  are  usually  infected  by  these  bodies — 
pus  is  formed.  (Fig.  57.)  Under  some  conditions,  as  in  debilitated  and 
neglected  children,  the  ulcerous  process  may  spread  rapidly,  as  in  the 
cheek  in  cancrum  oris;  or  when  specific  bacilli,  which  excite  much 
swelling  and  quick  death  of  the  tissues  of  the  cheek,  proliferate, 
causing  the  condition  called  noma. 

Prognosis.  Abscesses  tend,  as  a  rule,  to  spontaneous  cure  without 
marked  systemic  disturbance.  If  the  pus  discharge  persist  after 
evacuation  of  the  abscess,  persistence  of  the  cause,  or  infection  of  the 
abscess  walls  through  reinfection  or  by  retention  of  bacteria  in  the 
crypts,  is  to  be  suspected.    The  occurrence  of  rigors  (chills)  and  high 


92  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

fever  is  a  danger  signal.  A  fluttering,  weak  pulse,  and  clammy  extrem- 
ities indicate  profound  septic  intoxication,  and  are  indications  for  local 
disinfection  and  systemic  treatment. 

Treatment  of  Inflammation.  If  the  cause  of  inflammation  be  in 
evidence  it  must  be  removed;  good  examples  of  removable  causes  are 
a  splinter  in  the  flesh,  a  gangrenous  tooth  pulp,  etc.  Ordinarily  the 
pus  of  an  abscess  or  an  ulcer  contain  the  cause  (organisms)  within  it; 
therefore  the  pus  should  be  removed  by  opening  the  abscess,  if  its 
situation  can  be  determined,  after  which  the  pus  cavity  is  syringed  out 
with  antiseptics,  wdiich  destroy  the  pus  and  the  organisms.  Hydrogen 
dio^pde  in  3  per  cent,  aqueous  solution  is  commonly  used;  it  is  made 
more  effective  by  the  addition  of  mercuric  chloride  (1  :  1000). 

In  ulceration  the  pus  and  organisms  are  destroyed  in  a  similar 
manner,  though  at  times  sloughing  tissue  requires  removal  by  the 
curette,  caustic  agents,  or  by  digesting  agents,  as  caroid,  papoid, 
brewers'  yeast,^  etc. 

Dead  bone  acts  as  a  septic  irritant  and  requires  removal,  and  at 
times  an  abscess  will  remain  persistently  infected,  requiring  surgical 
removal  of  tissue.  The  abscess  or  ulcer,  if  protected  from  further 
infection,  usually  heals  by  formation  of  granulation  tissue.  A  deeply 
seated  abscess  may  require  to  be  packed  with  antiseptic  gauze  (noso- 
phen),  in  order  that  it  may  granulate  from  the  bottom  out. 

Ulcers  are  usually  dusted  with  antiseptic  powders,  iodoform,  aristol, 
or  nosophen,  which  cause  drying  of  the  surface  and  prevent  the  access 
or  action  of  organisms.  Under  certain  circumstances  the  presence  of 
suppuration  is  not  certain,  though  phlegmonous  (spreading)  inflam- 
mation is  somewhat  pathognomonic  of  it.  In  such  cases  hot,  moist 
applications,  such  as  hot  poultices,  soften  the  surface  above  the  abscess 
and  determine  its  direction  of  discharge,  thus  limiting  burrowing. 
Counterirritants  applied  directly  above  the  inflamed  area  also  hasten  in 
such  cases.  The  stimulation  may  aid  resorption  (destruction  by  phago- 
cytosis) of  the  pus  and  resolution  occur .^  The  vascular  engorgement 
in  an  inflamed  part  may  be  reduced  by  local  blood-letting. 

Nancrede  found,  on  dividing  a  vein  upon  the  distal  side  of  an  area 
of  inflammation,  that  after  a  brief  period  the  flow  of  blood  was  estab- 
lished through  the  inflamed  area.  Local  blood-letting  by  leeches 
(Gensmer)  produced  even  more  marked  effects.  Drugs  which  stimu- 
late the  vasoconstrictors  (ergot),  and  those  which  paralyze  the  con- 
strictors (aconite),  lessen  the  blood  pressure  in  the  inflamed  area;  so 

1  Park's  Surgery.  ■  -  Ibid, 


REGENERATION  OF  TISSUES.  93 

that  if  administered  in  the  early  stages  of  inflammation  they  may 
modify  its  severity.  If,  on  the  contrary,  they  are  administered  after 
stasis  occurs,  they  increase  the  stasis — ergot  actively  and  aconite  pass- 
ively. If  the  flow  of  blood  through  the  inflamed  area  be  re-established 
by  local  blood-letting,  then  the  arterial  sedatives  are  distinctly  useful 
in  lessening  the  flow  of  blood  to  the  part. 

When,  owing  to  vascular  engorgement,  throbbing  pain  is  a  promi- 
nent symptom,  applications  of  cold  are  useful  in  lessening  the  calibre 
of  vessels  and  in  relieving  pain.  But  if  there  be  firm  exudation  and 
marked  stasis,  cold  is  a  detriment.  Heat  then  gives  relief  through 
inducing  a  more  free  flow  of  blood  in  the  collateral  circulation.  Very 
hot  applications  act  as  do  cold  applications,  by  causing  contraction  of 
vessels,  and  may  be  used  to  abort  an  inflammation. 

In  certain  situations,  as  in  case  of  an  inflamed  tooth  pulp,  sedative 
applications,  antiphlogistics,  are  required.  Conjoined  with  local 
measures  of  reducing  vascular  engorgement,  the  use  of  counterirritants 
and  general  derivatives  are  indicated.    (See  Treatment  of  Hypersemia.) 

General  sedatives  are  at  times  demanded  for  the  relief  of  pain. 
Morphine  used  in  small  and  continued  doses  not  only  relieves  pain, 
but  causes  a  contraction  of  small  vessels.  Other  anodynes  are  also 
used  in  this  connection. 


REGENERATION  OF  TISSUES. 

Connective  tissues  that  have  been  lost  by  inflammatory  process  or 
operation  are  replaced  by  granulation  tissue  arising  by  mitotic  division 
of  cells  of  the  connective-tissue  group.  The  forms  of  healing  are  by 
first  intention,  second  intention  or  granulation,  healing  under  a  scab, 
and  healing  under  a  clot.  Epithelial  tissues  are  replaced  only  by 
multiplication  of  epithelial  cells.  The  forms  of  healing  are  practically 
alike  by  formation  of  granulation  tissue,  the  form  being  simply  a  modi- 
fication (of  extent)  of  healing  by  second  intention. 

Healing  by  Second  Intention.  Shortly  after  evacuation  of  pus  from 
an  abscess  the  process  of  repair  is  instituted.  The  leukocytes  come  to 
the  surface  of  the. wound  in  great  numbers;  some  of  these  may  degen- 
erate into  pus  cells.  Immediately  beneath  the  uninjured  connective- 
tissue  cells  multiply,  forming  embryonic  cells  (fibroblasts) ;  at  the  same 
time  the  endothelial  cells  of  the  capillaries  multiply  at  points,  throwing 
out  solid-pointed  projections  or  buds  from  the  sides  of  the  capillaries 
(Fig.  58,  b).     These  lengthen  and  join  buds  from  other  capillaries 


94 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


(Fig.  58,  c,  d,  e).  By  mitosis  the  nuclei  divide  horizontally,  lying  side 
by  side  (Fig.  58,  d).  Later  these  separate  into  two  cells,  discovering  a 
lumen  into  which  blood  enters  from  the  parent  capillary  (Fig.  58,  a/,  c). 


Eegeneration  of  capillary  bloodvessels:  o,  normal  cajjillaries;  6,  capillary  process;  C,  new 
capillary  appeai-ing' in  divided  process;  d,  process  undergoing;  division;  e,  connecting  cell  in 
which  no  sign  of  division  has  yet  appeared.     Diagrammatic.     (Green.) 


c'   o  Q  o 
.^    o    o  Q    o    Q  Q 


A  granulating  surface:  a,  layer  of  pus;  &,  granulation  tissue  with  loops  of  bloodvessels; 
e,  commencing  development  of  the  granulation  tissue  into  a  fibrillated  structure.  X  200. 
Diagrammatic.     (Rindfleisch.) 


REGENERATION  OF  TISSUES. 


95 


In  this  manner  loops  are  formed,  about  which  the  fibroblasts  are 
arranged  (Figs.  59  and  60). 

Together  these  form  minute  red  elevations  upon  the  surface  of  the 
abscess  cavity  or  wound,  called  granulations.  Repeated,  the  process 
gradually  fills  the  abscess  cavity. 

Naturally,  collapse  of  the  walls  or  apposition  of  cut  edges  of  a  wound 
lessens  the  amount  of  granulation  tissue  necessary;  hence,  in  the  latter 


Transverse  section  of  granulation  tissue  from  an  open  wound  -with,  fibropurulent  deposit : 
a,  granulation  tissue ;  &,  fibropurulent  deposit ;  c,  bloodvessels.    X  150.     (Ziegler.) 

case,  healing  by  first  intention  (with  a  minimum  amount  of  granulation 
or  scar  tissue). 

The  wound  having  been  filled  up,  epithelium  grows  from  the  sides 
and  covers  the  granulations  (Fig.  61,  e).  The  granulation  tissue,  at 
first  highly  vascular,  later  contracts,  and  many  vessels  are  obliterated 
so  that  it  becomes  whiter  than  normal  tissue. 


96 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


The  indifferent  embryonic  cells  may  have  the  function  of  forming 
any  of  the  connective  tissues.  If  cartilage  is  to  be  formed,  chondrifi- 
cation  takes  place  about  the  specialized  cells.  If  bone  is  to  be  formed, 
certain  cells  form  islets,  about  which  calcification  proceeds.  Nerves 
require  a  month  or  more  to  pierce  the  cicatricial  tissue  (Eichhorst).^ 

In  healing  beneath  a  scab  the  exudation  and  leukocytes  upon  the 
surface  of  the  wound  dry  into  a  scab  beneath  in  which  granulations 


Laparotomy  wound— sixteenth  day:  a,  epithelium;  b,  cerium;  c,  subcutaneous  fat ;  d,  vessels 
in  scar  tissue  of  corium;  e,  newly  formed  epithelial  layer;  /,  vessels  in  subcutaneous  scar 
tissue.     X -iO-    3Iodi fled  from  Ziegler.     (Green.) 

and  an  epithelial  covering  are  formed.  Later  the  scab  falls  off.  If 
prematurely  lost  the  granulations  are  exposed. 

In  healing  under  a  clot  the  clot  is  invaded  by  leukocytes,  which  have 
a  solvent  action  upon  it.  Granulation  tissue  forms  upon  all  sides  of  it, 
grows  into  it,  and,  at  the  same  time,  removes  it  by  resorption  (Fig.  62). 
If  the  clot  become  septic,  the  granulations  may  become  infected  and 
break  down. 

Healing  under  a  clot  is  the  form  commonly  seen  after  tooth  extraction. 

In  certain  cases  of  abscess  with  contracted  fistulas  or  openings  of 

*  Ziegler,  General  Pathology. 


INFLAMMATION  OF  BONE. 


97 


Fig.  62. 


discharge,  the  orifice  may  close  before  the  granulations  have  filled  the 
pus  cavity.  If  pus  or  an  excess  of  exudate  be  now  formed  within  the 
cavity,  a  second  discharge  may 
occur.  To  obviate  this  difficulty, 
abscesses  are  often  packed  with 
antiseptic  gauze,  so  that  healing 
may  occur  from  the  bottom  of 
the  cavity,  while  drainage  is 
assured.  In  other  cases  the  plac- 
ing of  a  tent  or  drain  tube  in  the 
fistula  together  with  asepsis  suf- 
fice for  the  attainment  of  the 
object. 


INFLAIOIATION  OF  BONE. 

"Active  inflammatory  changes 
may  occur  in  the  periosteum, 
the  medullary  canal,  the  medul- 
lary spaces  of  the  spongy  bone, 
and  the  Haversian  canals,  the 
compact  tissue  and  ground  sub- 
stance remaining  passive."^  The 
inflammation  is  termed  perios- 


Absoi-ption  of  blood  clot.  Section  through  the 
margin  of  a  clot  formed  among  the  tissues  by 
extravasation,  sho^ving  the  growth  of  granu- 
lations by  which  it  is  removed :  d,  a,  portions  of 
clot;  5,  6,  original  tissue;  c,  c,  granulations 
springing  from  the  original  tissue  and  projecting 


into  the  clot ;  d,  d,  ■wandering  cells  or  leukocytes 
titis,    osteomyelitis,    and    osteitis,      that  seem  to  have  taken  red  blood  disks  into 
,  (•        •  1  •  their  interior.     (Section  cut  in  gum  arable  and 

the  terms  reterrmg  to  the  pomt-  stained  with  hsematosyiin.)   x  aso.  (Black.) 
of  location  of  the  inflammation 

— i.  e.,  the  periosteum,  the  medulla,  and  the  spaces — the  bone  being 
involved  in  all  cases. 

Inflammation  of  bone  may  be  non- infective  or  infective;  the  latter  is 
usually  due  to  pyogenic  organisms — i.  e.,  suppuration  occurs. 

Proliferative  Periostitis.  This  is  a  proliferation  of  cells  of  the 
deeper  layers  of  the  periosteum  combined  with  emigrated  leuko- 
cytes.    A  node  is  thus  formed  which  may  ossify. 

Suppurative  Periostitis.  Pyogenic  organisms  may  enter  an  injured 
periosteum  or  one  weakened  by  previous  disease  {e.  g.,  by  scarlet  fever). 
The  origin  of  the  bacteria  is  by  way  of  the  blood,  either  directly  or  by 
way  of  the  medulla  (a  secondary  effect  of  osteomyelitis),  or  by  way 
of  the  skin. 


1  Schmaus  and  Ewing,  Pathology  and  Pathological  Anatomy. 

7 


98  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

Pus  forms  beneath  the  periosteum,  raises  it,  and  destroys  its  con- 
nection with  the  bone.  The  vessels  are  stretched,  damaged,  and 
thrombosis  occurs.  Superficial  necrosis  of  bone  results,  which  may  be 
total  if  other  sources  of  blood  supply  are  also  cut  off. 

Acute  Osteomyelitis.  This  is  a  suppuration  occurring  in  the  bone- 
marrow,  which  infects  the  bone  proper,  causes  much  thrombosis  of 

vessels,  coagulation  necrosis  of  bone 
^"^'  ''^^  cells,  and  may  rapidly  cause  much 

necrosis  of  medullary  tissue.  Oc- 
curring in  large  bones,  much  toxin 
is  produced,  which  may  rapidly 
cause  death.  The  organisms  and 
thrombi  formed,  becoming  emboli, 
v-.i-L-r.^A^^jiirVMi^  may    rapidly     lead     to     pyaemia.^ 

Trabecule  of  bone  with  perforating        Prompt     surgical     interference     is 

canals.    X  50.  ^  ° 

called  for. 

Inflammation  of  bone  may  lead  to  its  rarefaction  (rarefying  osteitis 
or  osteoporosis),  its  condensation  (condensing  osteitis  or  osteosclerosis), 
or  its  death  (necrosis  and  caries). 

Rarefying  Osteitis  (Osteoporosis) .  In  the  rarefying  process  which 
occurs  in  chronic  inflammation,  granulation  tissue  is  formed,  which 
enters  the  Haversian  canals  and  spaces  of  spongy  bone  and  destroys 
(resorbs)  the  bone.  They  thus  form  new  channels  between  the  spaces — 
perforating  canal  resorption  (Fig.  63).  With  suppuration  (ulceration) 
added,  the  granulations  break  down,  leaving  the  bone  as  a  dead, 
spongy,  or  honeycombed  mass.  This  is  caries  of  bone.  In  the 
early  stages  the  inflammation  may  cease,  and  the  bone  not  only  be 
restored,  but  condensed. 

Condensing  Osteitis  (Osteosclerosis).  In  chronic  inflammation, 
instead  of  rarefaction,  the  trabeculse  of  bone  may  increase  in  thickness, 
so  that  all  spaces  and  Haversian  canals  become  smaller.  The  bone 
becomes  very  compact,  and  if  built  up  in  excess  of  its  orginal  dimen- 
sions, constitutes  the  condition  known  as  exostosis.  Both  condensing 
and  rarefying  osteitis  occur  about  the  alveolar  process  and  the  roots  of 
teeth.     (See  Hypercementosis  and  Resorption.) 

Necrosis  of  Bone.  Necrosis  of  bone  following  rarefying  osteitis  is 
known  as  caries.  It  is  a  molecular  death  of  bone.  Subperiosteal  death 
of  bone  occurs  from  infective  periostitis,  and  is  due  to  the  compression 

1  Park's  Surgei-y. 


INFLAMMATION  OF  BONE. 


99 


of  vessels  by  the  exudation  and  to  thrombosis.  Nutrition  ceases;  death 
results.  The  dead  piece  is  demarked  by  a  line  of  leukocytes  (phago- 
cytes), solution  of  continuity  occurs  at  the  line  of  union  with  the  living 


Fig.  65. 


Section  of  bone  and  periosteum  covering  it :  B, 
bone ;  C,  outer  fibrous  layer ;  a,  inner  layer  of 
white  fibrous  tissue ;  0,  layer  of  osteoblasts,  some 
of  which  reach  the  bone  Tvith  their  prolonga- 
tions.    (Black.) 


Section  of  bone  and  periosteum  covering 
it:  o,  osteoclasts,  cells  that  absorb  bone; 
&,  surface  of  bone,  shoTving  fibres  of  peri- 
osteum penetrating  it  and  a  Howship  lac- 
una.    (Black.) 


bone,  and  the  piece  is  thrown  out  as  a  sequestrum.  The  solution  is 
effected  by  granulation  tissue  as  the  rarefying  process  above  cited. 
(See  Gangrene.) 


Lattice- work  figures  in  halisteresis.     (After  v.  Recklinghausen.) 


Resorption  of  Bone.  Under  conditions  of  chronic  inflammation 
bone  is  often  removed  by  neighboring  tissue  in  one  of  several  ways. 

Lacunar  Resorption.  In  this  form  the  bone  is  excavated  by  giant 
cells  into  bays  called  Howship's  lacunae,  which  may  enlarge,  or  later 


100 


DISTURBANCES  OF  THE  VASCULAR  SYSTEAI. 


a  reconstructive  action  may  occur  and  osteoblasts  may  fill  up  the  bays 
with  bone. 

Perforating  Canal  Resorption.  This  has  been  described  under 
Caries  of  Bone.  The  canals  connecting  medullary  spaces  are  enlarged 
by  the  granulation  tissue  formed  in  them  (Fig.  63). 

Halisteresis  Ossium.  In  this  form  of  resorption  the  bone  first 
undergoes  decalcification  and  the  matrix  is  later  removed  (Fig.  66). 


Fig.  68. 


.■;i'' 


M 


\ 


■Mi 


0  -f 


\V 


Jk--V^V 


SIS- 

':'■:■''"■■  ' .    JtA' 


Fig.  67. — Diagram  of  healing  fracture.  From  a  guinea-pig,  ten  days  after  injury:  A',  ends  of 
the  bone;  m,  marrow;   c,  i^eriosteal  callus;  d,  medullary  callus;  o,  osteoid  tissue.     X  6. 

Fig.  68. — The  same  preparation:  M,  myelogenous  callus;  P,  periosteal  callus;  K,  end  of  the 
bone;  t,  osteoid  trabeculae ;  o,  osteoblasts  in  rows ;  p,  thickened  periosteum.  X  250.  (Schmaus 
and  Ewing.) 

Regeneration  of  Bone.  Bone  lost  by  suppuration  is  first  replaced 
by  provisional  tissue  of  the  connective-tissue  type  in  which  appear 
osteoblasts.  Calcification  then  proceeds  under  superintendence  of 
these  (Figs.  67  and  68). 

FEVER. 

The  term  fever  is  applied  to  a  condition  the  most  prominent  feature 
of  which  is  an  elevation  of  the  bodily  temperature  above  the  normal, 
37°  C.  To  constitute  a  fever  this  rise  in  temperature  must  continue 
for  some  length  of  time. 

Causes.  Fevers  are  commonly  caused  by  the  presence  in  the  circu- 
latory fluids  of  substances  which  act  as  poisons  upon,  probably,  the 
nerve  centres  controlling  heat  production.     As  a  rule,  the  offending 


FEVER.  101 

substance  is  a  poison  generated  in  the  body  through  the  action  of  micro- 
organisms. The  character  and  type  of  the  fever  are  determined  by  the 
nature  of  the  offending  substances — i.  e.,  the  variety  of  infection. 

Classes.  Fevers  are  divided  into  periodical  or  continued,  according 
as  to  whether  there  is  a  periodical  fall  of  temperature  and  a  subsequent 
rise,  or  whether  the  fever  continues  practically  unabated  from  the  begin- 
ning to  the  termination  of  a  disease.  Fevers  are  classed  in  severity 
according  to  the  maximum  temperature  and  again  according  to  their 
duration.  A  temperature  of  100.5°  to  101.3°  F.  is  called  slightly  febrile; 
101.3°  to  103°  F.  moderate  fever;  103°  to  105°  F.  marked  fever.  A 
temperature  above  106°  F.  is  termed  h}^erpyi*exia. 

Symptoms.  The  most  characteristic  symptom  of  fever  is  the  eleva- 
tion of  temperature;  accompanying  this  there  is  an  increased  frequency 
of  the  pulse.  In  acute  inflammatory  diseases  the  pulse  is  full  and 
bounding,  the  eyes  injected,  the  bowels  constipated,  and  the  urine 
scanty,  containing  an  excess  of  urea.  On  standing,  the  urine  throws 
down  a  brick-dust  deposit  (urates).  In  fevers  of  a  lower  t\^e,  or  in 
many  fevers  which  begin  as  described,  the  high,  bounding  pulse  is 
succeeded  by  a  soft,  quick  pulse,  and  evidences  of  great  debility.  In 
fevers  in  which  the  temperature  runs  high  there  is  commonly  evidence 
of  intoxication,  more  or  less  delirium,  and  reflex  muscular  action.  With 
a  persistent  temperature  and  a  pulse  becoming  softer  and  more  fre- 
quent, there  is  increasing  debility. 

Pathology  and  Morbid  Anatomy.  In  all  cases  of  continued  high 
temperature  the  fat  of  the  body  rapidly  disappears  and  granular  degen- 
eration occurs  in  the  muscles  and  viscera  of  the  body.  If  the  fever  be 
long  continued  and  of  an  adynamic  type,  this  degeneration  may  become 
marked.  Its  occurrence  in  the  muscles  of  the  heart  is  common  and  is 
an  element  of  danger.  There  are  an  increase  in  the  amount  of  carbon 
dioxide  formed  and  exhaled  from  the  body,  and  an  increased  amount  of 
oxygen  inhaled.  This,  with  the  increase  of  urea,  the  product  of  the 
oxidation  of  nitrogenous  tissues  (muscles,  glands,  etc.),  indicates  that 
the  oxidation  of  the  tissues  is  largely  increased;  hence  the  elevation 
of  temperature.  As  repair  does  not  equal  waste  in  fevers,  the  nutri- 
tive processes  being_  profoundly  disturbed,  the  essential  elements  of  the 
tissues  suffer  from  the  increased  oxidation  and  undergo  degenerative 
changes. 

Prognosis.  The  higher  the  temperature  and  the  longer  it  continues, 
the  greater  drain  there  is  upon  the  vital  forces.  As  a  rule,  a  temperature 
of  106°  F.  persisting  more  than  twenty-four  hours  presages  death.    If 


102  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

the  vital  forces  flag  and  the  heart  action  becomes  weakened,  and  if 
there  be  evidence  of  profound  intoxication,  such  as  twitching  of  tendons, 
low,  muttering  delirium,  and  a  clammy  surface,  the  outlook  is  bad. 
Favorable  signs  are  falling  temperature,  a  clear  eye,  tongue  losing  its 
coating,  free  action  of  the  bowels,  free  perspiration,  free  action  of  the 
kidneys,  and  a  good  vascular  tension. 

Treatment.  In  the  light  of  present  knowledge,  efforts  should  first 
be  made  to  discover  the  nature  of  the  cause  of  the  fever  and  to  remove 
it,  if  possible.  If  not,  attention  should  be  directed  to  maintaining  the 
vital  forces  until  the  body  rids  itself  of  the  offending  causes.  As  many 
fevers  are  self-limited  in  course  and  duration,  this  latter  treatment 
becomes  an  important  consideration.  The  temperature  should  be  kept 
within  safe  limits  by  the  administration  of  antipyretics,  when  the  con- 
dition of  the  heart  will  permit  their  use,  and  also  by  cool  spong- 
ing or  cool  baths.  The  action  of  the  heart  should  be  sustained  by  the 
administration  of  concentrated  nutriment,  and  by  stimulants  when 
necessary.    The  bowels  must  be  kept  open. 

In  any  form  of  fever  there  is  no  therapeutic  measure  comparable 
with  the  removal  of  the  cause,  provided  this  be  discoverable,  identified, 
and  removable. 

TOX.ffi]yiIA. 

By  toxaemia  is  meant  a  more  or  less  general  disturbance  of  the 
economy  as  the  result  of  the  presence  in  the  blood  of  substances 
poisonous  to  a  tissue  or  the  tissues.  The  substance  may  be  a  normal 
constituent  of  the  blood  which  has  accumulated  owing  to  faulty 
elimination — e.  g.,  urea — or  be  derived  from  the  alimentary  canal  as 
the  result  of  unusual  fermentation  therein.  Such  an  effect  is  known 
as  autointoxication.  It  may  be  due  to  the  action  of  drugs  of  toxic 
character — e.  g.,  alcohol,  or  iodoform.  This  is  drug  toxaemia.  Again, 
it  may  be  due  to  the  action  of  the  products  of  bacteria,  which  products, 
absorbed  from  certain  foci  of  infection,  produce  general  effects,  such 
as  fever. 

Septic  Intoxication.  By  septic  intoxication  is  meant  the  absorption 
into  the  blood  of  the  products  of  bacterial  acti\dty,  which  products  are 
produced  at  some  focus  or  foci  of  infection  as  the  result  of  tissue  or 
tissue-juice  decomposition.  These  bacterial  products  produce  symp- 
toms of  general  poisoning  or  intoxication,  which  are  mild  or  severe, 
according  to  the  character  of  the  poisonous  body  produced.  The 
organisms  do  not   necessarily  enter   the   blood,  hence    the   blood   is 


SEPTICEMIA.  103 

not    infectious  if    inoculated   into  another   person   (or  experimental 
animal). 

Two  varieties  of  septic  intoxication  may  be  distinguished: 

1.  Intoxication  by  the  products  of  the  action  of  specific  bacteria 
developing  upon  living  tissue. 

2.  Intoxication  by  the  action  of  bacteria  upon  non-vital  materials 
(saprsemia). 

The  action  of  the  bacilli  of  diphtheria,  Asiatic  cholera,  and  tetanus 
are  examples  of  the  first  class.  Their  toxins  are  virulent,  but  the 
bacteria  are  confined  to  the  pharynx,  intestine,  and  the  wound, 
respectively. 

Saprsemia.  The  entrance  of  putrefactive  or  the  pyogenic  organ- 
isms into  such  material  as  a  large  blood  clot  or  gangrenous  area  may, 
by  putrefaction,  cause  the  formation  of  large  quantities  of  toxins. 
These,  if  absorbed,  produce  rapid  and  profound  symptoms  of  intoxi- 
cation. The  symptoms  vary  according  to  the  nature  of  the  toxin  and 
the  quantity  absorbed,  but  ordinarily  occur  in  the  following  order: 
malaise,  rigor,  fever  and  its  symptoms,  nausea,  vomiting,  headache, 
diarrhoea,  prostration,  delirium  in  some  cases,  muscular  weakness, 
clammy  skin,  feeble  pulse,  quick  respiration,  and  in  fatal  cases  coma 
and  death.  The  symptoms  are  similar  to  those  of  septicaemia,  but 
appear  more  rapidly — i.  e.,  septicaemia  requires  time  to  spread.  There 
is  a  putrid  wound  which  is  the  source  of  the  toxic  substance.  The 
condition  is  usually  complicated  by  septicaemia. 

SEPTICEMIA  (GENERAL  SEPTIC  INFECTION). 

By  septicaemia  is  meant  a  condition  in  which  the  bacteria,  usually 
one  of  the  pyogenic  varieties,  gain  entrance  to  the  living  tissues,  enter 
the  circulation,  and  are  carried  to  inaccessible  parts,  where  their 
development  continues  and  from  which  point  their  toxins  are  ab- 
sorbed (Fig.  69). 

This  process  requiring  more  time  than  mere  absorption  of  toxins, 
the  symptoms  are  much  more  delayed  than  in  sapraemia.  The  blood 
is  highly  infective  in  minute  amount,  as  it  contains  bacteria. 

Pathology.  There  is  a  septic  wound  in  which  incubation  occurs  for 
several  days.  The  lymphatics  leading  from  the  part  and  the  nearest 
lymphatic  glands  become  inflamed.  In  pronounced  cases  the  spleen 
is  enlarged.     There  is  marked  leukocytosis. 

Examination  made  after  death  from  the  septic  intoxication  pro- 


104  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

duced  by  both  saprjemia  and  septicaemia  exliibits  fairly  constantly 
enlargement  of  the  spleen  and  disintegration  of  tlie  red  corpuscles,  with 
staining  of  the  intima  of  the  vessels  and  heart.  The  lungs  are  con- 
gested.    Death  occurs  through  heart-failure.^ 

Symptoms.  These  are  similar  to  those  of  saprsemia,  except  that  the 
periods  of  incubation  about  the  body  cause  delays. 

Treatment  (for  Saprt^mia  and  Septicaemia).  The  treatment  is  both 
local  and  general.    The  local  treatment  involves  the  opening  and  dis- 


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W§. 

Pectoral  muscle  beset  -n-ith  large  numbers  of  the  streptococcus  pyogenes,  from  a  case  of 
phlegmonous  inflammation  of  the  subcutaneous  and  intermuscular  connective  tissue,  due  to 
cadaveric  poisoning  (the  phlegmon  of  the  wall  of  the  chest  developed  two  days  after  the 
finger  was  injured,  and  the  intermediate  lymph-vessels  of  the  arm  showed  no  e^•idences  of  being 
involved):  a,  perimysium  internum  full  of  streptococci;  6.  transversely  cut  muscular  fibres, 
still  intact;  c,  transversely  cut  muscular  fibres  which  are  beginning  to  degenerate;  rf,  muscular 
fibres  into  which  the  cocci  have  penetrated.  (Preparation  treated  with  gentian  violet  and 
vesuvin,  and  mounted  in  Canada  balsam.     Magnified  350  diameters.)      (Ziegler.) 

infection  of  all  wounds,  even  the  extirpation  of  a  part  and  of  neighbor- 
ing glands  being  sometimes  necessary  for  removal  of  the  cause.  If 
possible,  the  part  is  immersed  continuously  in  hot  water,  which  may 
occasionally  have  mercuric  chloride  added  to  it. 

An  antiseptic  salve,  consisting  of  resorcin,  5  parts;  ichthyol,  10  parts; 
unguentum  hydrarg>Ti,  40  parts;  lanolin,  45  parts,  is  to  be  applied  to 
the  area  of  infection. 

Crede's  silver  ointment  may  be  applied  to  the  unbroken  skin  for  the 
systemic  antiseptic  effect  of  the  silver.^ 

1  Green,  Pathology  and  Morbid  Anatomy.  -  Park's  Surgery. 


PYEMIA.  105 

The  general  treatment  consists  in:  1.  Clearing  the  alimentary  canal 
by  means  of  cathartics  and  maintaining  its  asepsis  by  means  of  mer- 
curic chloride  in  small  doses,  salol,  or  other  suitable  antiseptic.  2. 
Supporting  the  heart  action  by  means  of  alcohol  and  strychnine.  3. 
Supporting  the  strength  by  concentrated  liquid  nourishment,  such  as 
egg  albumen,  beef  peptonoids,  beef  juice,  peptonized  milk,^  to  which 
diet  fruit  may  be  added.^  4.  Reducing  the  temperature  by  means  of 
cold  sponge  baths  or  quinine.  5.  Maintaining  the  eliminative  action 
of  the  kidneys  until  the  system  has  rid  itself  of  the  toxins.  For  the 
more  profound  cases  Park  recommends  the  intravenous  infusion,  as  an 
intravascular  germicide,  of  from  500  c.c.  to  1000  c.c.  of  a  solution  of 
Crede's  soluble  silver,  1  :  1000  of  sterihzed  water  at  105°  F.  The 
value  of  streptococcus  antitoxin  is  still  not  proven. 

PY-fflMIA. 

By  pyaemia  is  meant  a  form  of  septicaemia  or  septic  infection 
by  pyogenic  organisms,  wliich,  locating  at  favorable  spots,  as  in 
the  capillaries,  multiply  and  produce  numerous  abscesses  known  as 
miliary  or  metastatic  abscesses.  From  these  foci  toxins  are  absorbed, 
which  produce  a  septic  intoxication. 

The  organisms  may  enter  the  blood  from  some  focus  of  suppuration 
as  free  cells  or  be  taken  up  by  leukocytes,  or  thrombosis  may  occur  at 
the  original  focus  of  infection  and  portions  of  clot  be  carried  in  the 
blood  as  septic  emboli  to  terminal  arteries,  where  the  results  of  septic 
infarction  are  set  up.     (See  Infarction.) 

Symptoms.  The  symptoms  of  pysemia  are,  in  general,  those  of 
septicaemia;  their  appearance  is  delayed  from  the  date  of  the  reception 
of  an  injury  or  the  outbreak  of  the  primary  suppuration.  The  onset 
of  pyaemia  is  usually  by  a  chill  or  a  succession  of  chills.  Each  fresh 
area  of  pus  formation  is  believed  to  be  announced  by  a  chill  and  a  rise 
of  temperature.  The  temperature  is  subject  to  remissions,  and  sudden 
variations  in  its  height  are  noted.  The  general  symptoms  are  those 
of  an  adynamic  fever.  Local  symptoms  appear  according  to  the  point 
of  lodgement  of  septic  emboli.  Pus  centres  may  be  found  in  the  lungs, 
and  cause  symptoms  of  dyspnoea;  collections  frequently  occur  in  joints, 
causing  loss  of  mobility;  eruptions  appear  on  the  skin,  the  swellings 
being  apparent;  typhoid  symptoms  become  more  pronounced,  and  an 
increasing  debility  ushers  in  a  usually  fatal  ending.  At  times  both 
septicaemia  and  pyaemia  may  become  chronic. 

1  Thompson's  Practical  Medicine  2  Park's  Surgery. 


106  DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 

Treatment.  The  treatment  of  pytemia  should  be  preventive.  The 
carrying  out  of  rigid  antiseptic  precautions  has  much  lessened  the 
frequency  of  pyaemia.  If  areas  of  infection  are  removable,  they  are 
removed  no  matter  what  extent  of  operation  may  be  necessary.  The 
general  treatment  is  the  same  as  in  septicaemia,  with  much  less  hope 
of  recovery, 

A  consideration  of  the  infective  surgical  processes  in  connection  with 
dental  and  oral  diseases  is  of  the  utmost  moment  to  the  practitioner  of 
dentistry.  Nearly  all  of  the  diseases  which  the  dentist  is  called  upon 
to  treat  are  infective  from  their  inception.  ^Moreover,  the  saliva,  hold- 
ing in  suspension  numerous  forms  of  bacteria,  both  saprophytic  and 
parasitic,  and  their  waste,  is  a  highly  infective  fluid. 

It  has  been  clearly  demonstrated  by  the  researches  of  ]\Iiller^  that 
many  forms  of  bacteria  found  in  specific  diseases,  and  found  inhabiting 
the  intestinal  tract,  are  more  or  less  constantly  present  in  the  human 
mouth,  and  that  the  pathway  in  many  general  infections  is  no  doubt 
via  the  oral  cavity.  A  wound  made  in  the  human  mouth  is  necessarily 
an  infected  wound.  In  the  vast  majority  of  cases  the  body  exercises 
its  protective  function  in  a  phagocytosis,^  which  disposes  of  invading 
bacteria.  In  other  cases  it  is  beyond  question  that  this  protective  pro- 
\dsion  fails  and  infection  occurs. 

THE  EXANTHEMATA. 

Certain  acute  specific  diseases,  such  as  rubeola,  rotheln,  scarlatina, 
varicella,  and  variola,  are  accompanied  by  skin  eruptions  generally 
distributed  over  the  body,  and  which  represent  an  infective  dermatitis ; 
indeed,  the  eruptions  of  many  of  these  diseases  are  contagious  to  other 
individuals.  Sj^philis,  a  chronic  specific  disease,  produces  similar 
effects. 

The  special  interest  lying  in  the  exanthemata  is  that  occurring  dur- 
ing the  development  of  the  teeth;  the  latter  are  often  profoundly  affected 
so  that  malformations,  sometimes  serious  in  character,  occur  in  the 
teeth.  It  is  to  be  recalled  that  teeth  are  dermoid  structures,  certainly  in 
so  far  as  the  enamel  is  concerned.  (See  Malformations  of  the  Teeth.) 
Again,  after  or  during  exanthematous  diseases,  notably  scarlet  fever, 
the  oral  tissues  are  much  debilitated,  so  that  abscesses  about  the  teeth 
may  produce  much  necrotic  tissue. 

'  Micro-organisms  of  the  Human  Mouth.  -  Hugenschmidt,  Dental  Cosmos,  1896. 


SECTION  II. 

EMBKYOLOGY,  ANATOMY,  AND  HISTOLOGY. 


CHAPTER   VI. 

THE  DEVELOPMENT,  ANATOMY,  AND  HISTOLOGY  OF  THE  JAWS 

AND  TEETH. 

As  malformations  of  the  parts  about  the  mouth  and  of  the  teeth  are 
dependent  upon  defective  development  of  the  same,  it  is  incumbent 
that  certain  facts  concerning  their  embryology  should  be  stated.  In 
like  manner,  as  the  processes  of  _ 

pathology  are  modified  by  the 
peculiar  anatomy  of  the  teeth 
and  associated  parts,  it  is  neces- 
sary that  a  previous  knowledge 
of  these  be  acquired  before  the 
special  dental  pathology  can  be 
comprehended.   The  embryology       ^^mt         ^  ^^^^^mi 

of  the  mouth   begins  at  a  very    iq^^R    _^^^^^^^^^^^P^ 3 

early  period — before  the  twelfth     g^^K. ^^^fff^^^^^^s 

day  the  future   mouth   may  be       ^^fc  "^V^HHi^^a  ^ 

located    (His,    Fig.    71).     Vhe     ^^^^—-^----^^^^^  6 

mouth  and  nasal  cavity  are  cir-         7^^^b= 

cumscribed    by  parts  which  are  ii^R-i^)fr 

developed    by   outgrowths   from 

the    head    fold    of    the     foetus.  9^E 

Those     structures     immediately       ^       ,         ,        .,,«,,. 

</  y  ace  oi   an  embryo  oi  twenty-nve  to  twenty- 

COncerned   are   the    lateral    tuber-  eight  days  (magnified  fifteen  times) :  1,  frontal 

1  •   •  J?  1  J*  1  prominence;  2,  3,  right  and  left  olfactory  fossse; 

CleS      arismg      trom      the      frontal  4,  inferior   maxillary  tubercles,   united   in   the 

prominence        fFiff        71)        which  ^^'^'^^s   Une;    5,    superior   maxUlary   tubercles; 

^  \      &•  /'  g^  mouth  or  fauces;  7,  second  pharyngeal  arch; 

grow  downward  and    fuse,  form-  S,  third;    9,  fourth;    10,  primitive  ocular  ves- 

,1  ,1  1  ,  icle;   11,  primitive  auditory  vesicle.     (Gray.) 

mg  the  nose,  the  nasal  septum, 

the  intermaxillary  bones,  and  anterior  portion  of  the  upper  Up  (Figs. 

72  and  73).     From  the   sides   of   the  head  fold   at   the  level  of   the 


108     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

mouth  and  neck  appear  certain  lateral  protuberances,  or  pharyngeal 
arches.  The  first  pharyngeal  arches  (Fig.  70,  4)  divide  into  (1)  the 
superior  maxillary  tubercles  (Fig.  70,  5)  and  (2)  the  inferior  maxillary 

Fig.  71. 


Sup.  tubercle 
Lateral  tubercle 


Sup.  tubercle 
Lateral  tubercle 


Head  of  an  early  human  embryo,  showing  the  disposition  of  the  facial  fissures  and  the  superior 
and  lateral  tubercles.     (His.) 


S.M.P.- 


S.M.P. 


NAS. 


Diagram  illustrating  scheme  of  union  of  the  processes.  JV.S.,  lateral  tubercles  forming  in- 
ternal maxillary  bones,  INT.  ^L■lX.,  and  nasal  septum.  S.M.P.,  superior  maxillary  processes 
forming  palatal  processes  of  superior  maxillse,  S.M.P.  N.C.,  nasal  cavity.  O.C,  oral  cavity. 
I.M.,  inferior  maxillary  processes  united. 

tubercles  (Fig.  70,  4,  shown  just  beneath  the  oral  cavity  and  united  in 
the  median  line). 

The  superior  maxillary  tubercles  develop  the  palate  bones,   the 


ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH.    109 


Fig.  73. 


Complete  bilateral  fissures  (coloboma)  of  face.     (Guersant.) 


Ftg.  74. 


Vertical  transverse  section  through  head  of  human  embryo,  about  the  tenth  week:  1,  nasa 
cartilage;  2,  buccal  cavity;  3,  tongue;  4,  dental  ridge,  lower  jaw;  5,  nasal  ca^^.ty;  6,  denta 
ridge,  upper  jaw;  7,  dental  ridge,  lower  jaw.     X  30.     (Bromell.) 


110    ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

superior  maxillae,  and,  with  the  aid  of  the  lateral  tubercles,  the  malar 
bones.  They  form  the  balance  of  the  upper  lip  (Fig.  73).  The  arch 
itself  forms  the  cheek. 

Secondary  processes  developing  horizontally  toward  each  other 
form  the  palatal  portions  of  the  superior  maxillae  and  palate  bones  and 
unite  at  the  median  line  (Fig.  72,  S.M.P.),  forming  the  vault  of  the 
mouth  and  floor  of  the  nasal  cavity.  Union  occurs  with  the  lateral 
processes  later  forming  the  intermaxillary  bones  and  bearing  the  germs 
of  the  incisor  teeth  (Fig.  75),  thus  completing  the  formation  of  the 
upper  jaw  and  lip. 


One  for  nasal  and 
facial  porlii,ns 


One  for  orbital  and 
malar  portions. 


Fig.  75. 


Anterior  Surface. 


At  birth. 


One  for  incisive 
portion. 


One  for  palatal 
portion. 


Inferior  Surface. 

Development  of  the  superior  maxillary  bone,  by  four  centres. 

The  inferior  maxillary  tubercles  grow  forward  and  unite  at  the 
median  line,  developing  the  inferior  jaw  and  lip. 

The  structures  of  the  floor  of  the  mouth  and  neighboring  structures 
are  formed  from  the  second,  third,  and  fourth  pharyngeal  arches  and 
a  tubercle  arising  near  the  first  pharyngeal  arch.  The  fusions  of  the 
lateral  portions  of  the  upper  maxillse  begin  first  anteriorly  at  about  the 
eighth  week  and  progress  posteriorly  until  complete  at  about  the 
eleventh.  Malformations  due  to  non-union,  therefore,  date  from  this 
period,  and  consist  of  the  following  typical  varieties: 

1.  Non-union  of  lip  and  of  maxilla  and  intermaxillary  bone  on  one 
side  (harelip,  Figs.  76  and  80). 


ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH,     m 


2.  Non-union  of  lip  and  intermaxillary  bone  on  both  sides  (double 
harelip,  Fig.  73). 

3.  Non-union  of  all  horizontal  processes  in  the  median  line  (cleft 
palate,  Figs.  76  and  77). 


Fig.  76. 


Fig.  77. 


Cleft  of  hard  and  soft  palate:  rudimentary  Cleft  of  hard  and  soft  palate.      (Mason.) 

intermaxillary  bone    placed  in  advance  of 
Ups.     (Mason.) 

Fro.  78. 


Median  fissure  of  the  lower  hp  and  chin.      (Marshall,  after  Wlifler.) 

4.  Non-union  of  halves  of  soft  palate  (cleft  velum). 

5.  Non-union  of  halves  of  the  uvula  (bifid  or  cleft  uvula). 
Combinations  of  cleft  velum  and  cleft  palate  or  of  cleft  palate  and 
single  or  double  harelip  may  exist. 


112     AX  ATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

The  failure  of  the  inferior  maxiUary  tubercles  to  luhte  is  rare,  but  is 
occasionally  seen  (Fig.  78).  The  inferior  maxillary  tubercles  develop 
a  transitory  support  to  the  lower  jaw  known  as  Meckel's  cartilage.  The 
cartilages  of  the  right  and  left  side  do  not  fuse  together  at  the  future 
symphysis  (Hertwig).     (Fig.  79.) 

It  acts  as  a  support  to  the  fetal  jaw,  undergoes  atrophy  at  about  the 
sixth  month  of  gestation,  and  at  birth  but  few  fragments  are  found 
near  the  symphysis. 

The  end  of  the  cartilage  in  the  base  of  the  inferior  maxillary  process 
becomes  the  future  malleus  (one  of  the  bones  of  the  middle  ear).  The 
portion  of  the  cartilage  running  from  the  malleus  to  the  formed  bony 
lower  jaw  becomes  transformed  into  the  internal  lateral  ligament  of 
the  inferior  maxilla  (Hertwig). 


Fig.  79. 


Fig.  80. 


M.C. 


Showing  Jleckel's  cartilage  (M.C.)    in 
longitudinal  and  transverse  section. 


Osteology  of  harelip.     (Museum  of  the 
Philadelphia  Dental  College.) 


It  is  to  be  remembered  that  these  processes  are  formed  by  the  meso- 
blastic  layer  of  the  blastoderm  and  are  covered  by  epithelial  tissue 
springing  from  the  epiblast.  Both  are  concerned  in  the  formation  of 
the  teeth.    Epithelium  is  reflected  over  the  face  and  oral  cavity. 


DEVELOPMENT  OF  THE  TEETH. 


The  first  evidences  of  tooth  formation  are  seen  at  about  the  sixth 
week  of  gestation,  at  a  period  when  the  superior  and  inferior  maxillary 
processes  are  but  ill-defined  masses  of  mesoblastic  tissue  surrounded 
on  all  sides  by  epiblastic  tissue.  Before  the  union  of  the  processes 
which  are  to  separate  the  nasal  from  the  oral  cavity  and  which  form 


DEVELOPMENT  OF  THE  TEETH.  113 

the  future  palate  is  complete,  the  first  evidences  of  tooth  formation  may 
be  observed.  It  is  to  be  borne  in  mind  that  during  the  entire  period  of 
tooth  formation  other  formative  changes  are  in  operation,  out  of  which 
arise  all  of  the  parts  associated  with  the  teeth. 

A  transverse  section  of  the  jaws  at  this  period  (Fig.  74)  exhibits  the 
following  features:  The  oral  cavity  is  as  yet  not  separated  from  the 
nasal  cavity  by  the  palatal  processes  of  the  superior  maxillae.  The 
tongue  is  seen  as  a  pear-shaped  body  attached  to  the  lower  jaw.  Over 
the  summit  of  the  lower  jaw  and  tongue  is  reflected  the  epithelium  of 
the  developing  mucous  membrane,  which  is  continuous  with  that  of 
the  cheeks  and  upper  jaw,  etc.  Over  the  outside  of  the  fetal  head  is 
reflected  the  epithelium  of  the  developing  skin.  These  epithelial 
structures  are  derived  from  the  epiblastic  layer  of  the  blastoderm. 

Fig.  81. 


Porcine  embryo:  ep,  epithelium,  infant  layer  or  stratum  Malpighu,   ct,  embryonal  connective 
tissue  with  large  intercellular  interspaces      134  cm.  X  250.    (Sudduth.) 

Between  the  epithelium  of  the  mouth  and  that  reflected  over  the  face 
is  seen  at  the  sixth  week  a  mass  of  indifferent  or  embryonic  cells 
(Fig.  81).  These  arise  from  the  mesoblastic  layer  of  the  blastoderm. 
Later  in  its  substance  are  seen  in  the  lower  jaw  two  elliptical  areas, 
the  sections  of  Meckel's  cartilage  (Fig.  82,  9).  Examined  more 
minutely  in  transverse  section  there  is  seen  at  a  point  upward  and 
outward  from  Meckel's  cartilage  and  outward  and  downward  from 
the  sides  of  the  tongue  (in  the  lower  jaw)  on  each  side  a  thickening  of 
the  epithelium  (Fig.  82,  4).  Active  multiplication  of  the  epithelial 
cells  at  this  point  has  caused  a  raising  of  the  epithelial  surface  and  a 
depression  of  the  stratum  Malpighii  (Fig.  81,  ep)  into  the  mesoblastic 
tissue  beneath  (Fig.  83,  h,  and  Fig.  85,  c).  This  extends  the  entire 
length  of  the  jaw  (Fig.  84,  6),  and  is  most  pronounced  at  the  anterior 


114     ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

Fio.  82. 


::  Vertical  transverse  section  through  head  of  human  embryo,  about  twelfth  week,  showing  the 
single  buccal  cavity  transformed  into  the  oral  and  nasal  ca\'ities:  1,  cartilaginous  septum  of 
nose;  2,  dental  ridge;  3,  oral  ca^■ity;  4,  dental  ridge;  5,  anlage  of  lower  jaw;  6,  nasal  cavity; 
7,  dental  ridge;  8,  tongue;  9,  Meckel's  cartilage.     X  30.     (Bromell.)     Compare  with  Fig.  74. 


Fig.  83. 


mr.  ep. 

Vertical  transverse  section  of  jaw  of  porcine  embrj'o,  showing  differentiation  of  periosteum: 
p,  periosteum  of  either  jaw;  e.el,  follicular  wall,  appearing  as  a  continuation  of  the  periosteum; 
6,  band;  eo,  enamel  organs  for  premolars;  ep,  epithelium;  db,  developing  bone;  vie,  Meckel's  car- 
tilage.    53^  cm.  ,  '  25.     (Sudduth.) 


DEVELOPMENT  OF  THE  TEETH. 


115 


portion,  thinning  toward  the  posterior.  The  elevation  is  the  dental 
ridge  (Fig.  82,  4,  7).  The  depression  was  named  by  Goodsir  the 
primitive  dental  groove,  a  name  now  obsolete.  To  the  continuous 
horseshoe-shaped  structure  the  name  ''band"  has  been  applied  (Fig. 
84,  6,  and  Fig.  85,  c). 

From  the  inner  side  of  the  band  at  regular  intervals  are  given  off  in 
each  jaw  ten  buds  or  dental  cords,  which  are  to  form  the  enamel  organs 


Fig.  84. 


o.t- 


Longitudinal  transverse  section  of  the  inferior  maxilla  of  a  porcine  embryo:  &,  band,  solid  at 
anterior  portion,  but  divided  posteriorly  into  band  and  lamina.     3  cm.  X  40.     (Sudduth.) 

of  the  twenty  deciduous  teeth.  The  order  of  formation  is:  1.  Central 
incisor.  2.  Lateral.  3.  First  molar.  4.  Second  molar.  5.  Cuspid 
(Magitot).  The  cords  grow  down  (down  means  here  away  from  the 
epithelium,  whether  up  or  down)  into  the  mesoblastic  tissue. 

A  small  sac  is  formed,  somewhat  constricted  at  the  neck,  and  con- 
taining in  its  interior  epithelial  cells.  This  is  the  enamel  organ  in  its 
first  or  saccular  stage  of  development^  (Fig.  86).  Up  to  the  ninth 
week  epithelial  cells  are  pushed  into  the  interior  of  the  enamel  organ 


1  Andrews,  American  Text-book  of  Operative  Dentistrj^. 


116      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

bv  multiplication  from  the  inner  sides  of  its  walls,  which  are  composed 
of  the  rete  jMalpighii.  An  interiorward  growth  of  cells  corresponds 
with  an  upward  growth  upon  the  mucous  membrane. 

Fig.  85. 


Vertical  section  through  band  from  jaw  of  porcine  embryo:  ep,  epithelium;  6,  band;  c,  cord; 
et,  connective  tissue.    3}4  cm.  X  60.     (Sudduth.) 


Fig.  86. 


Section  of  jaw,  embryo  of  pig,  showing  growth  of  enamel  organ:  1,  epithelium;  2,  stratum 
Malpighii;  3,  first  stage  in  growth  of  enamel  organ  of  temporary  tooth;  4,  embryonic  connec- 
tive tissue;  5,  de^'eloping  bone  of  jaw.     (Andrews.) 


DEVELOPMENT  OF  THE  TEETH. 


117 


By  this  means  the  enamel  organ  is  enlarged  at  its  lowest  portion, 
while  it  coincidently  remains  constricted  at  its  attachment  to  the 
mucous  membrane  (Fig.  87).  The  enamel  organ  thus  assumes  a  shape 
likened  to  a  Florentine  flask.  This  is  the  second  stage  in  its  saccular 
development  and  takes  place  from  the  ninth  to  the  twelfth  week 
(Magitot).    At  the  same  time  the  mesoblastic  tissue  condenses  about 


Fig.  87. 


Section  of  jaw,  embryo  of  pifj,  .■showing  growth  of  enamel  organ:    1,  epithehum;   2,  second 
stage  in  growth  of    enamel  organ;  3,  embryonic  connective  tissue.     (Andrews.) 


the  lower  part  of  the  enamel  organ,  begins  to  flatten  it  (Fig.  88),  and 
later  invaginates  it.  The  mesoblastic  tissue  directly  beneath  thus 
becomes  a  papilla,  over  which  the  enamel  organ  adapts  itself. 

From  the  twelfth  to  the  sixteenth  week  the  papilla  enlarges  and 
further  invaginates  the  enamel  organ,  which  is  reflected  over  it  (Fig.  89, 
sr  and  djp),  and  at  the  same  time  the  mesoblastic  cells  surrounding 
both  condense  into  a  fibrous  structure   (the  follicular  wall),  which 


118      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

entirely  surrounds  the  papilla  and  enamel  organ,  and  is  continu- 
ous with  a  developing  fibrous  structure  reflected  to  form  a  periosteum 
for  the  outer  surface  of  the  bone  of  the  jaw  (Fig.  89,  c,  ct,  and  p).  The 
follicular  wall  and  its  enclosures  constitute  the  dental  follicle.  This 
is  the  folhcular  stage  of  tooth  development.  At  points  between 
the  follicular  wall  and  periosteum  bone  develops  in  islets,  which  later 
coalesce.    This  is  the  interstitial  bone  formation  of  Sudduth. 

At  the  sixteenth  week  the  cord  of  the  enamel  organ  of  the  temporary 
tooth  gives  off  from  its  side  an  epithelial  bud  and  then  parts  from  the 


Fir,.  SS. 


.f«^'.. 


^NP, 


Section  of  jaw,  embryo  of  pig,  showing  growth  of  enamel  organ  and  zone  of  dentine-forming 
tissue:  1,  epithelium;  2,  enamel  organ;  3,  zone  of  dentine-forming  tissue.     (Andrews.^) 

enamel  organ.  This  bud  is  to  later  develop  the  enamel  organ  of  the 
permanent  tooth  (Fig.  89,  cp). 

From  the  twelfth  to  the  sixteenth  week  internal  changes  occur 
in  the  enamel  organ,  dentinal  papilla,  and  follicular  wall,  prepara- 
tory to  their  respective  functions  of  enamel,  dentine,  and  cementum 
deposition. 

The  developing  enamel  organ  consists  of  an  inner  and  outer 
Malpighian  layer  of  cells  with  epithelial  cells  enclosed. 

The  nucleated  cells  of  the  Malpighian   layer  lying  next   to  the 


1  American  Text-book  of  Operative  Dentistry. 


DEVELOPMENT  OF  THE  TEETH. 


119 


papilla  become  columnar  from  mutual  pressure  and  development,  and 
are,  apparently,  defined  at  their  ends  by  an  inner  and  outer  mem- 
brane (Fig.  90,  d,  c)   and  are  now  called  ameloblasts  (Fig.  90,  e). 


Fig 


Vertical  transverse  section  of  jaw  of  porcine  embryo,  injected:  ep,  epithelium,  with  {il)  infant 
layer;  a,  layer  of  ameloblasts;  o,  layer  of  odontoblasts;  q),  cord  for  permanent  tooth;  ot,  outer 
tunic;  it,  inner  tunic;  sr,  stellate  reticulum;  wh.  en.,  whorls  of  epithelium  formed  from  outer 
tunic  and  stellate  reticulum;  d,  dentine;  dp,  dentinal  pulp;  v,  bloodvessels  of  pulp;  ct,  connective 
tissue;  C.  ct.,  follicular  wall;  p,  periosteum;  sp,  space.     10  cm.  X  60.     (Sudduth.) 


Their  function  is  the  deposition  of  enamel.  Those  epithelial  cells 
lying  next  to  them  (interiorly)  in  the  enamel  organ  become  developed 
into  a  layer  known  as  the  stratum  intermedium  (Fig.  91,  6),  which 


120       ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

Williams  has  shown  to  have  later  in  the  rat  a  papilla-like  structure 
and  to  stand  in  nutritive  relation  to  the  ameloblasts  (Fig.  92).  In  the 
centre  of  the  enamel  organ  lie  nucleated  cells  made  polygonal  by  mutual 
pressure.     These  cells  constitute  what  is  known  as  the  stellate  retic- 

FiG.  90. 


Section  of  developing  tooth  of  an  embryo  calf:  a,  b,  nuclei  of  reticulum  of  enamel  organ, 
showing  spongiose  character;  c,  outer  ameloblastic  membrane;  d,  inner  ameloblastic  mem- 
brane; e, /,  enamel  globules  faintly  showing  nuclear  network.     X  1000.     (Williams.) 


ulum  (Fig.  89,  sr;  Fig.  90,  b),  and  have  been  showai  by  Sudduth  to 
disengage  carbon  dioxide  when  a  weak  hydrochloric  acid  is  allowed 
to  infiltrate  beneath  the  cover-glass,  thus  showing  the  presence  of 
calcium  salts.     Their  function  is  supposed  to  be  the  fabrication  of  the 


DEVELOPMENT  OF  THE  TEETH. 


121 


pabulum  for  the  first  deposition  of  enamel.    They  disappear  before 
the  entire  thickness  of  the  enamel  is  deposited. 

Within  the  papilla  changes  also  occur.  Upon  the  surface  next  the 
enamel  organ  appear  nucleated  elongated  cells  called  odontoblasts, 
the  function  of  which  is  to  deposit  dentine  (Fig.  89,  d;  Fig.  91,  e). 
Connective-tissue  cells,  nerves,  and  bloodvessels  also  develop  (Fig. 
89,  v;  Fig.  91,  /). 

Fig.  91. 


Section  of  developing  tooth  of  an  embryo  calf:  a,  stellate  reticulum  of  enamel  organ;  b,  stratum 
intermedium;  c,  ameloblasts;  d,  dentine;  e,  odontoblasts  ;  /,  bloodvessel — corpuscles  in  situ. 
X275.     (Williams.) 

The  follicular  wall  also  develops  and  contains  osteoblasts  and  other 
structures  peculiar,  to  itself,  to  be  described  when  treating  of  the  peri- 
cementum, which  the  follicular  wall  later  practically  becomes.  Its 
function  in  tooth  development  is  to  deposit  cementum,  which,  however^ 
does  not  occur  until  the  crown  of  the  tooth  is  formed.  While  the 
structures  which  are  to  form  the  hard  tissues  of  the  teeth  are  in  process 
of   development  there  appear  at  different   points  in  the  mesoblastic 


122      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

tissue,  situated  between  the  follicular  wall  and  the  periosteal  fibres, 
certain  cells  about  which  calcification  occurs.  It  is  probable  that  these 
cells  deposit  the  bone  about  pre-existing  fibres.  The  calcification  begins 
at  what  are  termed  islets  which  later  coalesce. 

With  an  understanding  of  the  development  of  these  three  structures 
and  of  the  formation  of  bone  in  islets,  the  student  is  prepared  to  grasp 
the  facts  connected  with  the  development  of  the  hard  and  soft  tissues 
of  the  teeth. 

Calcification.  Analyses  of  the  enamel,  dentine,  and  cementum  show 
them  to  be  composed  of  a  combination  of  inorganic  salts,  chiefly 
calcium  phosphate  and  carbonate  and  magnesium  phosphate,  and 
carbonate  with  an  organic  basis. 

Fig.  92. 


r^^:: 


-.  ^ 


'^'>A->       « 


Section  of  incisor  of  rat:  a,  capillary  loops  torn  out  of  secreting  papillae;  6,  secreting  papillae  after 
removal  of  capillary  loops;  c,  ameloblasts;  d,  enamel;  e,  dentine.     X  80.     (Williams.) 


The  experiments  of  Harting,  Rainey,  and  Ord  have  shown  a 
reaction  which  no  doubt  has  a  direct  bearing  upon  the  formation  of  all 
calcified  tissues.  If  to  an  albuminous  solution  a  solution  of  a  calcium 
salt  be  added,  the  calcium  enters  into  chemical  combination  with  the 
albumin,  forming  a  substance  indefinitely  known  as  albuminate  of 
calcium,  and  called  by  its  discoverer  calcoglobulin.  If  calcium 
carbonate  be  formed  in  a  solution  of  albumin,  the  above  combination 
occurs,  making  definite  structural  forms,  minute  laminated  spheres, 
which  are  called  calcospherites;  these  spheres  coalesce  and  form 
laminated  masses — i.  e.,  form  in  layers.  When  exposed  to  the  action 
of  dilute  acids  these  spherites  are  more  resistant  than  the  crystallized 
salts;  moreover,  after  the  action  of  the  acid  the  form  of  the  spherite 


DEVELOPMENT  OF  THE  TEETH.  123 

remains.  This  chemical  fact,  the  union  of  crystalloidal  with  colloidal 
substances,  is,  no  doubt,  of  wide  significance  in  general  and  special 
pathology,  for  it  is  extremely  probable  that  the  formation  of  all  path- 
ological concretions  is  an  expression  of  some  such  reaction.  The 
evidence  is  strong  that  calcium  albuminate  is  the  basis  of  all  of  the 
calcic  tissues;  but  precisely  where  its  formation  occurs  in  enamel 
formation  is  unknown;  presumably,  it  occurs  or  is  completed  in  the 
enamel-forming  cells,  the  ameloblasts. 

It  is  to  be  remembered  that  the  materials  composing  bone,  enamel, 
dentine,  and  cementum,  while  of  one  family,  differ  as  to  the  propor- 
tions of  their  constituents. 


Fig.  93. 


A 


:i 


\\S   /'vj  J)  1  i  .    ::'  il   XiH 


^r,  i''^ 


j'CV.: 


lit  l^'vMf/liWtM  ::■;';  . 

Section  of  growing  tooth  of  calf  at  birth,  showing  fibrils,  fibril  cells,  and  odontoblasts;  also  the 
layer  of  calcoglobulin  and  the  forming  dentine.    (Andrews.) 

Dentinification.  The  first  deposition  of  calcific  material  occurs  with 
the  dentine  at  about  the  seventeenth  or  eighteenth  week  (Magitot). 

The  odontoblasts  upon  the  surface  of  the  papilla  are  apparently  of 
two  kinds:  (1)  fibril  cells  which  have  the  function  of  developing 
tubules,  and  (2)  other  odontoblasts  apparently  concerned  in  the 
development  of  intertubular  substance. 

The  deposition  of  dentine  has  been  variously  described.  Mummery 
has  demonstrated  that  between  the  odontoblasts  appears  a  delicate 
network  of  connective-tissue  fibres  derived  from  the  connective-tissue 
cells  of  the  pulp,  which  are  in  close  relation  to  the  odontoblasts.  These 
fibres  are  surrounded  by  a  protoplasmic  fluid.  Into  the  fluid  the 
odontoblasts  secrete  calcospherites,  small  globular  bodies  capable  of 
further  calcification  or  of  hardening  in  situ.    These  are  pressed  closely 


124      AX  ATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

against  each  other,  largely  obliterating  the  connective-tissue  matrix. 
Andrews^  terms  this  layer  of  unharclened  calcospherites  calcoglobulin 
(Fig.  93).  This  either  hardens  or  is  further  calcified  into  formed 
dentine  (Fig.  92,  e).  This  process  must  also  occur  about  the  proto- 
plasmic prolongations  from  the  fibril  cells  which  are  left  in  the 
dentinal  tubules  as  fibrillse.  As  these  fibrillse  have  later  the  power 
under  irritation  of  adding  substance  to  the  inner  wall  of  the  tubule 
(tubular  calcification),  it  is  probable  that  they  are  the  real  formers 
of  the  tubule  wall.  Additional  evidence  of  the  mode  of  deposition  is 
aflforded  by  observation  of  the  points  of  arrested  development  in 
dentine — i.  e.,  interglobular  spaces.  These  contain  a  partially  calcified 
matrix  material,  and  upon  the  borders  of  the  defects  are  seen  globular 
masses.  The  tubules  run  as  independent  formations  through  the 
matrix  material.     (See  Interglobular  Spaces.) 

The  first  deposition  of  dentine  occurs  against  the  inner  ameloblastic 
membrane  and  represents  the  future  external  portion  of  the  dentine 
of  the  crown.  The  deposition  occurs  first  at  a  point  beneath  the 
location  of  the  future  cusp  or  cusps,  which  are  supplied  by  the 
enamel  organ.  The  dentine  of  the  root  is  formed  first  against  the 
inner  side  of  the  follicular  wall,  which  later  supplies  the  cementum. 

The  first  layer  deposited,  the  odontoblasts  and  fibril  cells  recede, 
the  latter  leaving  a  protoplasmic  prolongation  in  the  dentinal  tubule. 

After  an  appreciable  portion  of  the  crown  is  formed  the  papilla  is 
called  the  pulp,  and  continues  to  form  dentine  and  to  recede  from  the 
neighborhood  of  the  ameloblasts,  until  the  dentine  of  the  root  is 
formed  (to  be  later  described),  when  it  practically  ceases  its  formative 
function,  unless  pathologically  excited,  and  persists  as  the  dental  pulp. 
In  this  latter  stage  its  normal  function  is  nutritive  rather  than  formative 
(Figs.  96,  98,  and  100). 

Amelification.  Shortly  after  the  deposition  of  the  first  layers  of 
dentine  the  ameloblasts  deposit  enamel  upon  the  dentine. 

Williams  has  shown  that  bubbles  of  carbon  dioxide  are  developed 
simultaneously  in  the  cells  of  the  stellate  reticulum,  the  stratum  inter- 
medium, and  the  ameloblasts,  when  a  mineral  acid  is  applied. 

The  inference,  therefore,  is  that  the  stellate  cells  give  up  pabulum 
to  the  cells  of  the  stratum  intermedium,  which  elaborate  it  and  pass 
it  to  the  ameloblasts. 

Within  the  ameloblasts  are  to  be  seen  two  classes  of  globular  bodies 
which  stain  differently.    The  first  class  consists  of  one  or  more  bodies 

1  American  Text-book  of  Operative  Dentistry. 


DEVELOPMENT  OF  THE  TEETH. 


125 


of  like  size,  which  are  only  found  at  points  between  the  nucleus  and 
the  end  of  the  cell  proximating  the  dentine  (the  proximal  end),  and 
are  connected  by  strings  of  protoplasmic  material.  These  are  the 
enamel  globules  (calcospherites)  inferred  by  Wilhams  to  arise  by 
mitosis  of  the  nucleus  of  the  ameloblasts  (Fig.  94,  E).  The  second 
class  of  bodies  are  ghstening  droplets  of  various  sizes,  which  coalesce, 
becoming  larger  as  they  approach  the  proximal  end  of  the  cell. 


Fig.  94. 


Mode  of  enamel  deposition:  ^.formed  enamel;  £,  ameloblasts;  C,  secreting  papillae  of  stratum 
intermedium;  D,  bloodvessels  in  external  fibrous  coat  and  to  secreting  papillae;  E,  enamel 
globules  with  connecting  plasmic  strings;  F,  nuclei  of  ameloblasts;  &,  blood  supply  of  odonto- 
blastic layer;  H,  odontoblasts  ;  I,  unformed  dentine;  /,  formed  dentine.  Semidiagrammatic. 
(Williams.) 

Wilhams  has  found  these  droplets  also  in  the  stratum  intermedium. 
This  substance  he  named  the  interprismatic  cement  substance.  The 
droplets  and  the  globules  are  the  materials  from  which  the  ameloblast 
constructs  the  enamel  rod  under  its  superintendence,  and  are  both 
calcoglobulin.  They  differ,  however,  in  that  later  the  globules  have 
a  crystalhne  structure,  while  the  cement  substance  is  amorphous.  The 
ameloblast  extrudes  first  against  the  previously  formed  dentine  a  droplet 
of  interprismatic  cement  substance,  and  into  this  it  also  deposits  an 


126       ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

enamel  globule;  as  these  two  substances  are  not  in  a  hard  condition 
when  deposited,  in  order  for  it  to  become  the  mature  enamel,  some 
change  must  take  place.  Noyes^  assumes  the  position  that  the  amelo- 
blasts  remove  any  organic  matter  present  in  the  calcoglobulin  (globules 
and  cement  substance),  depositing  calcific  matter  in  place  of  it. 

It  would  be  reasonable  to  infer  this,  as  enamel  contains  little  if  any 
organic  matter. 

After  the  first  layer  of  enamel  is  deposited  more  cement  substance 
is  extruded  and  a  second  globule  is  deposited  directly  atop  the  first. 
Mutual  pressure  causes  the  globules  to  assume  an  hexagonal  shape 
viewed  transversely,  and  also  reduces  the  interprismatic  cement 
substance  to  a  minimum.  The  record  of  this  process  is  to  be  seen  in 
the  sections  of  finished  enamel. 

The  ameloblasts  lie  at  an  angle  to  the  developing  enamel  rods  and 
also  preserve  their  integrity  to  the  end;  hence  the  rods  are  not  formed 
by  a  process  of  calcification  of  the  ameloblasts  themselves,  but  by 
a  process  of  deposition  of  calcified  materials  under  the  superintendence 
of  enamel  cells. 

As  soon  as  the  first  layers  of  enamel  have  formed,  a  notable  change 
is  seen  to  occur  in  the  enamel  organ;  the  stellate  reticulum  disappears 
over  the  forming  enamel.  The  calcic  material  stored  in  its  cells  has 
been  exhausted  in  forming  the  first  layer  of  enamel;  the  succeeding 
enamel  has  a  different  source  of  formative  material.  The  stellate 
reticulum  atrophies  and  the  outer  boundary  wall  of  the  enamel  organ 
comes  into  apposition  with  the  stratum  intermedium.  Williams  observed 
in  the  enamel  organs  of  rodents  (Fig.  92)  that  the  cells  of  the  stratum 
intermedium  become  arranged  over  loops  of  vessels  from  the  follicular 
wall,  so  that  papillae  are  formed.  He  infers  that  a  similar  arrangement 
occurs  in  the  enamel  organ  of  man;  and  that  the  function  of  the 
papillary  structure  is  the  selection  from  the  blood  plasma  of  ma- 
terial to  be  passed  into  the  ameloblasts  and  out  of  which  enamel 
is  formed. 

Enamel  and  dentine  formation  proceed  during  the  rest  of  fetal  life 
and  in  advance  upon  the  tips  of  the  papilla  or  pulp,  gradually  extend- 
ing down  its  sides.  At  birth  the  process  is  not  complete,  the  crown 
dentine  being  but  two-thirds  formed  and  the  enamel  lacking  the  lustre 
of  mature  enamel. 

Constant^  points  out  that  the  proper  lustre  is  not  imparted  before 

1  American  Text-book  of  Operative  Dentistry. 
-  International  Dental  Journal,  June,  1903. 


DEVELOPMENT  OF  THE  TEETH. 


127 


resorption  of  the  roof  of  the  crypt  takes  place — perhaps  at  five  months 
after  birth  for  the  central  incisors. 

Upon  the  surface  of  the  erupted  tooth  is  found,  after  special  treatment 
with  dilute  acids,  a  delicate  membrane  said  by  Kolliker  to  be  .,  ^  \  n  q  inch 
in  thickness,  known  as  Nasmyth's  membrane.  It  is  considered  by 
Andrews^  to  be  the  remains  of  the  ameloblasts  which  have  undergone 
partial  calcification. 

Hopewell-Smith^  dissents  strongly  from  this  view,  and  apparently 
demonstrates  his  position  that  it  is  an  epithelial  remnant  of  the  enamel 
organ  which  may  have  a  diameter  of  -^  inch,  and  which  consists  of 
a  translucent  layer  nearest  the  enamel,  upon  which  is  superimposed 
a  layer  containing  epithelial  cells. 

Fig.  95. 


1,  tooth  sacs  of  deciduous  teeth  turned  out  of  crypts;  2,  lingual  surface  of  mandible.     The 
interior  of  the  crypts  and  septa  shown.     (Bromell.) 

Ossification.  During  fetal  life  the  bone  develops  in  islets 
between  the  follicular  walls  and  the  periosteum.  These  islets 
coalesce  for  mutual  support.  Between  the  several  follicular  walls 
and  over  the  outer  edge  of  the  dental  follicle  bone  also  develops, 
so  that  the  jaw  may  be  considered  as  a  gutter  of  bone  divided  into 
cells  by  septa  of  bone  and  roofed  over  by  the  folhcular  wall  and  gum 
tissue  (Figs.  95  and  96). 

In  these  cells  or  crypts  lie  the  dental  follicles.  The  follicle  wall  is 
attached  to  the  pulp  only  at  its  base,  and  between  their  other  portions 
is  a  fluid.^  A  transverse  section  of  a  crypt  and  its  contents  is  shown  in 
Fig.  96. 

Cementification.  Root  Formation.  The  forming  crown  is  grad- 
ually pushed  by  the  forces  bringing  about  eruption  (which  see)  toward 


1  American  Text-book  of  Operative  Dentistry. 

2  Histology  and  Patho-histology  of  the  Teeth. 


3  Constant. 


128       ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 

the  gum,  and  root  formation  begins  after  practical  completion  of  the 
enamel.  Fig.  98  shows  that  at  six  months  after  birth  a  portion  of  the 
roots  of  the  anterior  teeth  is  formed;  at  birth  the  crown  was  not  com- 
pleted.   This  much  of  root  formation  has,  therefore,  been  completed 

Fig.  96. 


-^ 


A,  developing  bone;   B,  tissue  reflected  from  follicular  wall  and  forming  alveolar  periosteum; 
C,  follicular  wall;  D,  vessels  and  nerves;  E,  epithelium  of  gum. 

during  the  six  months.  After  birth  the  state  of  the  root  end  at  eruption 
demonstrates  a  very  large  apical  foramen  occupied  by  a  soft 
pulp  filled  with  bloodvessels  (Figs.  97,  100,  and  101).     At  the  exit 

Fig.  97. 


Pulp  cavities  of  the  superior  first  bicuspid,  from  the  seventh  to  the  twelfth  year.      (Bromell.) 

from  the  root  the  pulp  is  attached  to  the  follicular  wall,  which  is 
reflected  up  the  sides  of  the  root  (Figs.  96  and  100).  Between  these 
two  cementification  and  dentinification  are  accomplished  by  a  process 
analogous  to  enamel  and  dentine  formation  in  the  crown. 


DEVELOPMENT  OF  THE  TEETH. 


129 


The  pulp  forms  a  layer  of  dentine  extending  beyond  the  enamel. 
On  the  inner  surface  of  the  follicular  wall  and  between  its  fibres  appear 
a  row  of  osteoblasts,  bone-forming  cells  which  are  here  given  the  name 
of  cementoblasts,  and  these  deposit  cementum  (a  modified  bone)  upon 


Fig.  98. 


22  months  after  birth    - 
18  months  after  birth      — -^ 


12  months  after  birth 


6  months  after  birth 


40th  week  (birth) 
30th  week  embryo 


18th  week  embryo 
17th  week  embryo 


Calcification  of  the  deciduous  teeth.      (Peirce.) 


the  formed  dentine.  They  contain  glistening  bodies  which  they  extrude 
against  the  formed  dentine  and  then  retire.  Some  of  them  become 
included  in  the  cementum  by  the  deposition  of  cementum  about  them. 
They  persist  thus  as  bone  corpuscles  in  lacunse  connected  by  canaliculi. 


Fig.  99. 


Section  of  bone  and  periosteum  covering  it:  B,  bone;  c,  outer  fibrous  layer;  a,  inner  layer 
of  white  fibrous  tissue;  0,  layer  of  osteoblasts,  some  of  which  reach  the  bone  with  their  pro- 
longations.    (Black.)  ^  i 

The  second  layer  of  cementum  is  deposited  upon  the  first  and  so  on 
at  increasing  distances  from  the  dentine.  The  pulp  deposits  dentine  as 
in  the  crown,  at  increasing  distances  from  the  first-formed  dentine  and 
the  cementum.     As  the  crown  rises  through  the  gum  and  into  place 

9 


130      ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AXD  TEETH. 

in  the  arch,  more  root  is  buih  in  the  same  manner  until  a  type  is  reached. 
During  this  process  the  folHcular  wall  becomes  partly  drawn  up  with 
the  tooth,  and  the  alveolar  bone  fills  in  about  the  root.  The  follicular 
wall  is  thus  attenuated  and,  remainino;  attached  to  the  cementum,  is 


Fig.  100. 


Fig.  101. 


Condition  of  third  molar  at  thirteen  years  of  age. 
(Skiagraph  by  Custer  ) 

known  as  the  pericementum  (Fig. 
100 j.  There  is  some  evidence  that 
the  pulp  may  assume  root  form  in 
advance  of  calcification,  ocular  in 
the  case  shown  in  Fig.  102,  inferen- 
tial in  cases  of  fusion  by  the  roots. 
(See  Malformations  of  the  Teeth.) 

In  the  development  of  multirooted 
teeth  the  follicular  wall  plays  a  part. 
The  downward  growth  of  the  tooth 
pulp  is  counteracted  at  definite 
points  by  an  upward  development 
of  the  follicular  wall.  As  a  result 
the  pulp  is  invaginated  and  is  divided 
into  two  or  more  portions,  which  are 
to  become  the  pulp  filaments  of  the 

individual  roots.     Around  each  of  these  dentine  and  cementum  are 

formed  as  in  any  single-rooted  tooth,  while  the  upgrowth  of  follicular 

wall  develops  the  cementum  of  the  bifurcation  as  well  as  the  sides  of 

the  roots. 

There  is  evidence  that  a  lateral  division  of  the  pulp  may  occur  in 

the  same  manner.     The  cementum  so  formed   has  been  termed  by 

Bromell   interdentinal  cementum  (Fig.  103). 
The  Development  of   the  Permanent  Teeth.     At  the  fifteenth 

week  of  fetal  life  the  cords  for  the  first  permanent  molars  are  given 


Diagram  illustrating  root  development 
and  condition  of  an  incomplete  root:  E, 
enamel;  D,  dentine;  P,  pulp  containing 
odontoblasts,  OB;  AP,  alveolar  process; 
B,  bone;  C,  cementum;  P',  periosteum 
of  bone  continuous  with  the  pericementum; 
PEE,  pericementum  containing  cemento- 
blasts,  CB;  A,  V,  S,  arteries,  veins,  and 
nerves. 


DEVELOPMENT  OF  THE  TEETH. 


131 


off  from  the  epithelium  of  the  mouth.  Their  development  proceeds 
exactly  as  with  the  temporary  teeth,  and  at  the  twenty-fifth  week  the 
cap  of  dentine  appears  (Magitot). 


Fig.  102. 


Development  of  deciduous  incisor,  from  human  foetus:  1,  epithelium  of  jaw;  2,  dental  ridge; 
3,  dentine  papilla;  4,  calcified  dentine;  5,  enamel;  6,  outer  enamel  epithelium;  7,  germ  for 
permanent  incisor.     (Geise.) 

Fig.  103. 


Transverse  section  through  fused  roots  of  molar  tooth,  showing  interdentinal  cementum: 
1,  interdentinal  cementum.     X  30.      (Bromell.) 


132      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 


The  cords  for  the  permanent  incisors,  cuspids,  and  bicuspids  are 
given  off  at  the  sixteenth  week  from  the  side  of  the  cords  of  their 
temporary  predecessors,  and  their  foUicles  occupy  a  position  at  first 


Fig.  104. 


Fig.  105. 


Showing  the  relation  of  perma- 
nent tooth  follicle  to  the  root  of  the 
temporary  tooth. 


Tooth  folhcles  for  deciduous  and  permanent  teeth, 
three  months  after  birth:  1,  2,  tooth  sacs  of  deciduous 
teeth;  3,  periosteum  of  hard  palate;  4,  tooth  sacs  of  per- 
manent teeth.     (Bromell.) 


hngual  to  the  temporary  folUcle  and  later  Ungual  to  and  above  the 
root  of  the  temporary  tooth  (Figs.  104  and  105),  except  in  the  case 
of  the  bicuspids,  which  lie  in  the  bifurcations  of  the  temporary  molars 
at  a  later  period  (Fig.  106). 


Fig.  106. 


Deciduous  molars  ■vsith  tooth  sacs  for  permanent  bicuspids  attached  to  the  gingival  tissue. 

(BromeU.) 

The  process  of  crown  and  root  development  in  the  permanent  teeth 
is  the  same  as  for  the  deciduous  teeth,  but  proceeds  much  more  slowly 
(Fig.  107). 

It  will  be  seen  from  the  above  data  that  forty-four  teeth  are  in 
process  of  development  at  birth. 

At  three  months  after  birth  the  cord  for  the  second  molar  arises 


DEVELOPMENT  OF  THE  TEETH. 


133 


n      m 

to 

m 

m 

years, 
years, 
h  wee 
mbryo 

^       c3 

01 

(5) 

03 

rt 

>i      >> 

>, 

>, 

>, 

>. 

0  00 

1  i-H 

o 

(N 

o 

OJOO'O 

from  that  of  the  first  molar,  and  at  three  years  of  age  the  cord  for  the 
third  molar  arises  from  that  of  the  second  molar.^ 

The  temporary  teeth  are  completely  formed  in  a  period  averaging 
about  three  years  (Fig.  96).    The 
permanent  teeth  require  from  ten 
to  seventeen   years,  as    may  be 
seen  by  reference  to  Fig.  107. 

As  the  temporary  teeth  erupt, 
the  germs  of  the  permanent  teeth 
become  more  deeply  seated  and 
are  enclosed  in  crypts  of  bone  at 
a  point  lingual  to  and  above  the 
roots  of  the  temporary  teeth.  The 
bicuspids  lie  between  the  roots 
of  the  temporary  molars. 


Later  Development  of  the  Maxillae. 

Parri  passu  with  the  develop- 
ment of  the  teeth,  which  require 
increased  space  for  their  accom- 
modation, the  jaws  enlarge  in 
all  dimensions  in  correspondence 
with  development  in  the  other 
bones  and  tissues  of  the  body. 
In  common  with  these,  resorp- 
tions and  redepositions  of  tissue 
occur,  so  that  the  child's  jaw  is  in 
all  probability  entirely  removed 
and  redeposited.  In  no  other 
way  can  the  change  of  positio*n 
and  size  of  the  ramus  be  ac- 
counted for.  The  alveolar  pro- 
cess is  evidently  resorbed  and  re- 
deposited  at  least  once  (during 
second  dentition),  and  but  httle 
of  the  lower  infant  jaw  is  left  to 
be  considered.  The  same  process 
must  occur  about  the  maxillary 
sinus  in  the  upper  jaw  to  account 


1  Peirce,  American  System  ofJ[Deiitistry. 


134      ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AXD  TEETH. 

for  its  enlargement,  and  ^his  with  the  enlargement  of  the  various 
processes  by  probably  the  same  process  completes  the  development. 
Reference  to  Fig.  109  with  Fig.  110  and  Fig.  66  demonstrates  this. 

Fig.  108. 


Representing  a  jaw  of  a  nine  months'  fcetus,  superimposed  on  an  adult's  jaw,  to  show  in  what 
directions  increase  has  taken  place.     (Tomes.) 


Fig.  109. 


Showing  the  relative  sizes  of  jaws  at  the  age  of  two  years  and  in  the  adult. 


During  development  the  alveolar  process  is  widened  and  deepened, 
and  the  body  of  the  bones  enlarges  in  all  directions. 


DEVELOPMENT  OF  THE  TEETH. 


J  35 


Histology  of  the  Mature  Teeth, 

For  purposes  of  description^  human  teeth  may  be  defined  as  hard 
bodies  of  definite  form  implanted  in  the  maxillary  bones  and  gums, 
attached  thereto  by  membranes  and  subservient  to  the  purposes  of 
mastication,  facial  contour,  and  assistance  in  speech. 

That  portion  of  a  mature  tooth  in  position  and  not  implanted  is 
known  as  the  crown,  that  implanted  is  the  root;  the  point  at  which 
these  join  is  the  neck  or  cervix.  The  loosely  constructed  bone  by 
which  the  roots  are  supported  is  the  alveolar  process,  and  the  socket 
is  known  as  the  alveolus.  The  tooth  is  attached  to  the  alveolar  process 
by  a  tough,  fibrous  membrane,  the  pericementum  (Fig.  111).     The 


Fig.  110. 


View  of  the  upper  jaw  of  a  child,  aged  about  six  and  one-half  years.  The  anterior  teeth  are 
slightly  separated  by  the  partially  developed  permanent  teeth,  lying  behind  or  posterior  to 
them,  pushing  forward  to  occupy  a  more  anterior  position.  The  equal  height  which  the  crowns 
of  the  deciduous  originally  occupied  is  also  being  disturbed  by  the  advancing  permanent  teeth. 

tooth  may  be  said  to  be  composed  of  three  hard  and  three  soft  structures. 
These  are:  (1)  the  dentine,  forming  the  bulk  of  the  tooth;  (2)  the 
enamel,  covering  the  dentine  of  the  crown ;  (3)  the  cementum,  covering 
the  dentine  of  the  root ;  (4)  the  pulp,  occupying  a  central  cavity  in  the 
crown  and  root  dentine,  known  respectively  as  the  pulp  chamber  and 
root  canal ;  (5)  the  pericementum,  covering  the  cementum  and  attaching 
it  to  the  alveolar  process;  (6)  Nasmyth's  membrane,  found  on  the 
enamel  of  newly  erupted  teeth  and  later  mostly  worn  off. 

For  further  description  it  may  be  stated  that  a  periosteum  covers  the 
outside  of  the  alveolar  bone  and  body  of  the  maxilla.    Over  this  upon 


136      ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AXD  TEETH. 


the  alveolar  process  lies  submucous  tissue,  and  upon  this  raucous 
membrane  composed  of  a  corium  with  its  papillae,  covered  in  turn  by 
epithelial   cells.     The  gum  tissue   is   projected   somewhat   over  the 

Fig.  111. 


Ap.] 


Diagram  of  the  fibres  of  the  peridental  membrane:  6.,  gingival  portion;    Al.,  alveolar  portion; 
Ap.,  apical  portion.     From  a  photograph  of  a  section  from  incisor  of  sheep.    (Noyes.') 

enamel,  is  known  as  the  free  gingival  margin,  and  the  slight  free  space 
between  is  known  as  the  gingival  space. 

1  American  Text-book  of  Operative  Dentistry. 


DEVELOPMENT  OF  THE  TEETH. 


137 


Enamel.  The  enamel  is  a  hard  substance  covering  the  crown  of  a 
tooth  and  lying  directly  upon  the  dentine,  from  which  in  the  dried 
specimen  it  may  readily  be  removed.  It  is  thickest  at  the  cusps  and 
thinnest  at  the  cervix  of  the  tooth.  It  is  composed  chemically  of 
calcium  phosphate,  some  calcium  and  magnesium  carbonate,  and  a 
small  percentage  of  calcium  fluoride,  all  combined  probably  with  a 
minute  quantity  of  organic  matter  and  water  of  crystallization.  As 
stated  by  Noyes,  the  scheme  of  enamel  formation  involves  first  the 

Fig.  112. 


Diagram  of  enamel-rod  directions,  from  a  photograph  of  a  buccolingual  section  of  a  superior 

bicuspid.     (Noyes.) 


deposition  of  calcoglobulin  by  the  ameloblasts ;  later  these  cells  remove 
all  or  nearly  all  organic  matter,  replacing  it  with  inorganic  salts.  A 
longitudinal  section  of  enamel  shows  it  to  be  made  up  of  rods  of  a 
wavy  or  even  gnarled  outline,  radiating  in  the  main  from  the  dentine 
to  the  exterior  of  the  crown.  These  rods  subjected  to  force  cleave 
apart  longitudinally. 

Microscopic  examination   shows  the  indi\adual    rods  to  be  made 
up  of  globular  bodies  (enamel  globules)  set  end  to  end  like  a  string 


138      AXATOMY  AXD  HISTOLOGY  OF  THE  JAWS  ASD  TEETH. 

of  beads.    Between  tiiese  globules  is  seen  a  eementing  substance  lying 
transversely  to  the  axis  of  the  rod,  and  between  the  rows  of  globules 

Fig.  113. 


Section  of  enamel  of  human  toijiL.  i  .•...,;, ..i-lied  with  Zeiss  apochroniatic  lens  and  Powel 
and  Leland  apochromatic  condenser.  The  optical  parts  accurately  centred  and  the  focus 
"  critical."  The  enamel  rods  are  seen  to  be  resolved  into  distinct  sections  (enamel  globtiles), 
the  cement  substance  often  passing  entirely  between  the  sections.     )<  400.     (Williams.) 

Fig.  114. 


Enamel  prisms:  A,  fragments  and  single  fibres  of  the  enamel  isolated  by  the  action  of  hydro- 
chloric acid;  B,  surface  of  a  small  fragment  of  enamel,  showing  the  hexagonal  ends  of  the 
fibres.     X  350. 


is  more  of  the  material  known  as  interprismatic  cement  substance 
(Williams).     (Fig.  113). 
In  transverse  section  the  rods  present  an  hexagonal  appearance  due 


DEVELOPMENT  OF  THE  TEETH. 


139 


to  mutual  lateral  pressure  of  their  globules  during  development. 
Between  the  rods  is  seen  interprismatic  cement  substance. 

Recalling  the  embryology  of  enamel,  this  arrangement  of  enamel 
globules  and  interprismatic  cement  substance  is  seen  to  be  the  rational 
outcome  of  such  a  mode  of  deposition. 

Section  of  an  individual  globule  has  been  made  by  Mummery  and 
shows   a   centrosome-like,  crystalline   arrangement  of  its   molecules.^ 

Fig.  115. 


Incisor  tip,  sliowing  stratification  or  incremental  lines.     Rods  at  A  were  fully  formed  at  the 
time  the  rods  at  B  were  beginning  to  form.     X  80  (about).     (Noyes.) 

The  interprismatic  cement  substance  so  far  as  known  is  amorphous. 
Both  are  originally  calcoglobulin,  but  the  cement  substance  is  more 
soluble  in  dilute  acids.  These  penetrate  between  the  rods,  assisting 
their  cleavage  arid  strongly  marking  the  transverse  interprismatic 
cement  substance. 


1  Kirk,  lecture  before  the  Philadelphia  Academy  of  Stomatology. 


140      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH 


In  the  sulci  of  crowns  the  enamel  rods  may  be  separated — i.  e.,  not 
deposited  in  part  owing  to  persistence  of  Nasmyth's  membrane  in  that 
locality  (Fig.  112). 

The  enamel  of  human  teeth,  and,  indeetl,  that  of  animals,  differs 
in  the  relative  amount  of  cementing  substance  and  the  number  of 
globules,  and,  again,  in  the  regularity  of  the  distribution  of  the  two. 
In  one  specimen  the  globules  may  so  predominate  that  the  cementing 
substance  shows  in  sections  as  fine  lines ;  in  others  the  globules  may  be 
small,  rounded,  and  surrounded  l^y  a  relatively  large  volume  of  cement- 
ing substance.  Again,  at  different  parts  of  the  enamel  rods  both 
arrangements  as  to  relative  amounts  of  the  two  substances  may  be 
seen. 

Fig.  116. 


Enamel  showing  both  striation  and  stratification.     X  80  (about).     (Noyes.) 

The  enamel  rods  are  crossed  at  an  angle  by  transverse  brown 
bands  known  as  the  strife  of  Retzius,  which  are  parallel  with  one 
another. 

They  are  pigmentary  markings  representing  periods  of  enamel 
increment,  also  termed  developmental  lines. 

They  are  most  abundant  in  the  thickest  portions  of  enamel,  least 
so  in  the  thinnest — i.  e.,  more  or  fewer  incremental  periods  have  been 
required  for  completion.  Strata  are  also  noted  at  times  in  addition 
to  the  striae  of  Retzius. 

Another  set  of  cloud-like  markings  are  seen  by  reflected  light  as 
stripes  crossing    both    the    rods    and  striae  of    Retzius.     These  are 


DEVELOPMENT  OF  THE  TEETH. 


141 


explained  by  Caush^  as  due  to  the  presence  of  tubes  between  the 
enamel  rods,  as  will  be  shortly  described.  They  are  the  stripes  or 
lines  of  Schreger  in  enamel  (Fig.  117.)  The  enamel  globules  in  the 
area  are  normal. 

Williams  was  unable  to  make  enamel  take  up  staining  reagents 
except  at  isolated  spots,  which  he  regarded  as  accidental.  He  occa- 
sionally found  dentinal  fibrillse  extending  into  the  enamel  (Fig.  185), 
but  regarded  the  arrangement  as  a  malformation.  He  concluded 
that  enamel  was  without  nutrient  spaces.  More  recently  Caush, 
by  means  of  special  technique,  staining  both  by  external  application 


Ftg.  117. 

^M 

4 

y 

'1 

^"^pP 

Enamel  and  dentine,   human  tooth:   1,   enamel;   2,  dentine;   3,  lines  of  Schreger  in  enamel; 
4,  brown  striae  of  Retzius.     (Bromell,  after  Geise.) 

and  from  the  pulp  chamber,  has  succeeded  in  showing  the  existence 
of  tubular  structures  in  the  enamel  ("  enamel  tube"),  and  which  run 
from  the  dentine  out  and  from  the  surface  in.  He  found  them  also 
in  the  teeth  of  animals.  Fibrillar  connections  were  seen  to  enter  the 
tubes  next  the  dentine,  which  contained  a  material  taking  up  stain, 
and,  therefore,  considered  uncalcified.  Caush,  therefore,  regards  the 
enamel  as  endowed  with  nutrient  spaces,  by  which  he  accounts  for 
the  staining  of  enamel  by  copper  and  other  amalgams  placed  in 
cavities  of  decay.  If  his  contention  be  true,  it  may  explain  several 
of  the  phenomena  connected  with  the  enamel. 

1  International  Dental  Journal,  June,  1904. 


142      AXATOMY  AND  HISTOLOGY  OF  THE  JAWS  AM)  TEETH. 

The  color  of  implanted  teeth  sometimes  chano;es  to  that  of  the  other 
teeth.  This  cannot  be  due  to  a  nutritive  change  under  the  influence 
of  the  pulp,  as  it  is  removed  in  such  cases. 

Phvsiologically  the  enamel  is  a  protective  covering  for  the  dentine. 
It  is  insensitive — resistant  to  ordinary  wear,  practically  impervious  and 
highly  resistant  to  acids  generated  in  the  mouth  except  when  concen- 
trated upon  particular  spots,  as  in  caries  or  erosion. 

Nasmyth's  Membrane.  This  is  a  thin  membrane  ^i^  inch  or  less 
in  thickness  found  upon  the  enamel  of  newly  erupted  teeth,  but  later 
worn  off  by  friction.  It  may  be  removed  from  the  enamel  for  study 
by  the  use  of  a  10  per  cent,  solution  of  hydrochloric  acid.  It  is 
regarded  as  the  persistent  remains  of  the  enamel  organ  (Figs.  127 
and  130). 

Fir;,  lis. 


Longitudinal  ground-section  through  the  crown  of  a  cuspid  of  a  man  aged  twenty-three 
years.  Wet  ground-section  stained  by  Golgi's  method:  J,  interglobular  space;  S,  enamel. 
X  250.     (RUse.) 

The  Dentine.  The  dentine  forms  the  great  bulk  of  the  hard  tissues 
of  the  tooth  and  is  bounded  by  the  enamel,  the  cementum,  and  the  pulp. 

Its  substance  is  seen  upon  section  to  be  composed  of  tubules  and 
their  contents  and  intertubular  or  basis  substance.  There  is  from 
four  to  ten  times  as  much  basis  substance  as  of  tubules.  The  latter 
have  an  outside  diameter  of  from  22000"  *o  -g-iyVo  inch.  The  tubules 
pursue  a  curved  course  from  the  pulp  cavity  to  the  periphery  of 
the  dentine,  where  they  divide  dichotomously  and  may  anastomose. 


DEVELOPMENT  OF  THE  TEETH. 


143 


Those  curves  nearest  the  pulp  are  termed  primary,  those  farther 
away  secondary.  In  the  crown  they  radiate  from  the  pulp;  in  the 
root  they  lie  at  right  angles  to  it  and  are  less  curved.  They  are 
seen  upon  transverse  section  to  be  round  or  oval  in  outline,  and  to 
have  a  central  opening  or  lumen  (Fig.  119). 

Longitudinal  sections  show  that  this  lumen  contains  a  protoplasmic 
prolongation  of  a  fibril  cell  from  the  row  of  odontoblasts  upon  the  pulp 
surface  (Fig.  120).  This  prolongation  is  called  a  Tomes  fibre  or 
fibrilla  and  extends  the  entire  length  of  the  tubule.  The  tubule  wall 
surrounding  it  is  known  as  the  sheath  of  Neuman  (Fig.  119,  N.Sch.). 


Fig.  119. 


S^Sc/i. 


Transverse  ground-section  through  the  dental  tubules  of  the  first  molar  of  a  child  aged  seven 
years.      V,  Koch's  and  Golgi's  methods  combined.      ,<  1200.      (Rose.) 

The  tubule  walls  are  seen  in  both  sections  (Figs.  118  and  119)  to  have 
transverse  processes  connecting  them.  These  stain  like  the  tubule 
walls,  but  have  not  been  shown  to  contain  central  fibres. 

Tomes  and  Noyes  call  attention  to  the  fact  that  these  transverse 
tubules  are  scarce  in  the  proximal  (pulpal)  ends  of  the  tubules  in  the 
crown,  but  numerous  in  the  distal  ends  of  the  crown  tubules  and 
throughout  the  length  of  the  tubules  in  the  root  dentine. 

Lines  are  observed  in  some  specimens,  of  dentine  having  a  general 
parallelism  to  the  pulp.  They  run  at  right  angles  to  the  axis  of  the 
tubule  and  are  due  to  short  bends  in  the  length  of  many  adjacent 
tubules,  occurring  on  one  general  plane.  They  may  be  interpreted 
as  due  to  changes  of  direction  assumed  by  the  odontoblasts  in  tubule 


144      AX  ATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

building  at  the  particular  period.    Salter  has  termed  them  "incremental 
lines."    They  are  known  as  the  lines  of  Schreger  in  dentine. 

It  has  been  shown  by  Hart^  that  the  basis  substance  of  dentine  is 
traversed  by  a  fine  network  of  fibres,  a  connective-tissue  stroma  in 
which  the  calcific  process  occurs  (Fig.  121).'  Rose^  regards  these 
as  the  gelatin-yielding  fibres  of  the  dentine.     The  demonstration  of 

Fig.  120. 


C.D.- 


U.D 


P.O. 


T.F. 


Od. 


Section  of  pulp,  showing  the  relations  of  the  odontoblasts  to  the  dentine;  Od.,  odontoblasts' 
T.F.,  Tomes'  fibres — odontoblastic  processes;  V.D.,  uncalcified  dentine;  CD.,  calcified  dentine* 
P.C.,  pulp  cells.     X  800.     (Riise  and  Gysi.) 

Mummery  that  a  connective-tissue  stroma  is  seen  forming  in  advance 
of  calcospherite  deposition  in  dentine  formation  is  worthy  of  atten- 
tion as  corroborative  evidence.     (See  Dentinification.) 

In  the  border-ground  between  dentine  and  enamel  and  dentine  and 
cementum  the  dentine  may  present  a  different  histological  appear- 
ance from  the  general  mass  of  the  dentine.  Instead  of  the  orderly  sub- 
division of  the  dentinal  tubules,  this  portion  of  the  dentine  may  be 


1  Dental  Cosmos,  1891. 


Ibid.,  1902. 


DEVELOPMENT  OF  THE  TEETH.  145 

occupied  by  irregular  spaces — interglobular  spaces  in  which  the 
fibrillee  may  expand.  This  particular  layer  of  tissue  was  named  by 
its  discoverer,  Sir  John  Tomes,  the  granular  layer  (Fig.  122,  J).  As 
he  pointed  out,  the  layer  is  much  more  marked  beneath  the  cementum 
than  beneath  the  enamel. 

Interglobular  spaces  are  also  found  in  the  body  of  the  dentine.  (See 
Fig.  118  and  Malformations  of  the  Teeth.) 

Anatomically  the  dentine  is  the  tissue  composing  the  bulk  of  the 
tooth.     It  is  a  tissue  receiving  nourishment  from  the  pulp  via  the 

Fig.  121. 


Main  mass  of  dentine  of  a  temporary  tooth,  stained  with  chloride  of  gold,  decalcified  with 
acetic  acid:  F,  F,  dentinal  fibres,  partly  vacuoled;  B,  B,  basis  substance,  traversed  by  a 
reticulum.      X  1200.      (Hart.) 

fibrillse  and  through  the  same  is  capable  of  warning  sensations  and  of 
some  vital  reaction  to  causes  threatening  its  disintegration.  Under 
stimulus  the  fibrillse  may  produce  sclerotic  changes  in  the  dentine 
(tubular  calcification.) 

In  a  vital  condition  the  fibrillse  and  pulp  preserve  the  translucency 
of  the  tooth. 

The  Pulp.  The  pulp  is  the  highly  developed  remainder  of  the, 
dentinal  papilla. 

It  consists  of  a  gelatinous  matrix  containing  branched  connective- 

10 


146      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

tissue  cells,  a  type  of  tissue  known  as  myxomatous  (Fig.  119).  This 
is  traversed  by  bloodvessels  and  nerves  which  enter  by  way  of  the 
apical  foramen  and  subdivide,  breaking  up  finally  into  a  closely  inter- 
lacing plexus  of  non-medullated  nerve  fibres  and  a  capillary  network 
near  the  surface  of  the  pulp  (Figs.  123  and  124).  Over  the  entire 
surface  is  arranged  a  layer  of  nucleated  columnar  cells.  These  are 
the  odontoblasts. 

Fir,.   122. 


mm  ii 


■rf-^^^ 


i»-?SirJl'*' 


fmmm 


W    ( 


H-i     I  I  '  .       Jill 

Ground-section   through  the  ruut  uf  a,  Iiuiii:iii  preiiiular;    2>,  dentine;   A',  cement   corpuscles;   0, 
osteoblasts;  Ep,  pericemental  glands  of  Black;'  J,  interglobular  spaces.     X  200.     (Rose.) 

The  latter  send  prolongations  into  and  throughout  the  length  of  the 
tubules  of  the  dentine.    These  are  the  Tomes  fibres  or  fibrillae. 

One  or  more  arteries  enter  the  apical  foramen  or  by  several  fora_ 
mina,  and  several  veins  may  emerge.  The  arteries  subdivide  in  the 
central  portion  of  the  pulp  and  form  a  rich  network  of  capillaries 
beneath  the  odontoblasts. 

The  arteries  of  the  pulp  soon  lose  almost  entirely  their  muscular 
coat,  and  their  external  coat  is  reduced  to  an  inconsiderable  amount 
of  fibrous  connective  tissue;  the  veins  remain  for  an  unusual  distance 


1  The  editor  takes  the  liberty  of  altering  the  interpretation. 


DEVELOPMENT  OF  THE  TEETH. 


147 


without  a  muscular  coat.  This  histological  datum  has  great  clinical 
significance.     (See  Diseases  of  Pulp.) 

The  vascularity  of  the  pulp  decreases  with  age.  "In  young  teeth 
there  are  a  number  of  arterial  trunks  entering  the  apical  foramen, 
which  lessen  in  number  as  the  passage  lessens  in  size."    (Black.) 

The  passage  of  arteries  and  veins  through  a  constricted  foramen  has 
important  consideration  in  connection  with  pulp  diseases.  (See  Venous 
Hypersemia  of  the  Pulp.) 

The  nerves  enter  by  several  bundles  and  if  medullated  soon  lose  the 
medullary  sheath.  They  are  derived  from  the  trigeminus  and  the 
sympathetic  system. 


Fig.  123. 


Margin  of  dental  pulp:  a,  a,  dentinal  fibrils,  pulled  out  of  the  dentine;  b,  b,  membrana  eboris 
or  layer  of  odontoblasts;  c,  c,  transparent  zone  between  the  odontoblasts  and  the  cells  of  the 
pulp  proper;  d,  d,  layer  of  cells  closely  packed  together;  e,  e,  bloodvessels;  /,/,  cells  less  closely 
placed  toward  the  central  portions  of  the  pulp,    Wales'  immersion,  Vio-inch  objective.    (Black.) 

Those  from  the  sympathetic  are  distributed  to  the  bloodvessels  as 
vasomotors;  the  others  form  a  plexus  in  intimate  relation  with  the 
odontoblasts.  They  have  been  found  by  Retzius  to  terminate  in 
knob-like  extremities  between  the  odontoblasts  in  the  mouse.  These 
are  probably  sensory  nerves. 

No  direct  anatomical  connection  has  been  made  out  between  the 
nerve  fibres  and  the  odontoblasts  or  the  fibrillse,  although  Robertson 
has  claimed  to  have  traced  the  long  central  fibre  running  from  the 
odontoblasts  into  the  pulp  into  nerve  bundles  and  claims  that  they 
become  axis  cylinders.     The  phenomenon  of  sensitive  and  hyper- 


148      ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AM)  TEETH. 

sensitive  dentine  shows  an  evident  j)liysiolooical  connection.  The 
nerves  of  the  pulp  do  not  possess  tactile  sense.  The  pulp  contains 
no  demonstrable  lymphatics,  and  if  absent  their  office  is  probably 
performed  by  the  veins,  which  in  other  parts  may  take  up  this  function.* 
The  pulp  l)ecomes  more  fibrous  and  less  vascular  with  age. 

During  its  health  it  preserves  the  translucency  of  the  tooth  through 
its  relations  with  the  fibrillar,  and  under  certain  circumstances  renews 
its  formative  activity  and  produces  secondary  dentine. 


S.D.. 


Od.- 


N.T.- 


B.V 


Section  of  a  tcMith-piil;.:  U.  W.  iiiaiii  bliM.dve-j^els  of  pulp;  r,  <,nfiui  o!  capillaner-;  A.  T..  main 
nerve  trunk;  N.  F.,  subdivisions  of  nerve  into  fibrillar;  Od.,  odontoblastic  layer;  S.  D.,  secondary 
dentine;   C.  G.,  masses  of  calcoglobulin.     X  30.     (Riise  and  Gysi.) 

The  forms  of  the  pulp  and  the  pulp  cavities  are  shown  in  Chapter 
VII. 

The  Cementum.  The  cementum  is  a  modified  bone  distributed 
over  the  root  of  the  tooth.  It  meets  the  enamel  edge  to  edge.  In  some 
cases  it  overlaps  the  enamel  and  in  others  is  overlapped  by  it. 
(Choquet.) 


1   Green,  Pathology  and  Morbid  Anatomy. 


DEVELOPMENT  OF  THE  TEETH. 


149 


It  is  thinnest  at  the  cervix  of  the  tooth,  at  which  point  the  first 
layers  are  formed,  and  thickest  at  the  apex  and  in  the  bifurcation  of 
the  roots.  It  is  thicker  in  the  aged.  During  development  some  of 
its  formative  cells,  the  osteoblasts,  are  caught  in  its  substance,  persist- 
ing in  lacunse  with  their  canaliculi.  This  is  true  of  thick  lamellae,  not 
of  thin  ones,  as  of  the  cervix. 

Fig.  125. 


Two  fields  of  cementum,  showing  penetrating  fibres:   Gt,  granular  layer  of  Tomes;    C,  cementum 
not  showing  fibres;   F,  penetrating  fibres.      X  54  (about).      (Kirk.) 

There  is  evidence  of  stratification,  evidencing  periods  of  increment 
(Figs.  122  and  125),  and  the  remains  of  pericemental  fibres  which 
have  undergone  calcification  are  seen  as  numerous  fine  lines  running 
at  right  angles  to  the  axes  of  the  strata.  These  lines  represent  old 
points  of  attachment  of  the  pericemental  fibres  (Sharpey's  fibres) .  In 
some  cases  the  dentinal  tubules  of  the  root  terminate  in  the  cementum, 
but,  as  a  rule,  terminate  in  the  granular  layer  of  Tomes. 


150      ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND  TEETH. 

The  physiological  function  of  the  cementum  is  to  afford  a  means 
of  attachment  of  the  teeth  to  the  maxillary  bones  through  the  medium 
of  the  pericemental  fibres.  In  case  of  death  of  the  pulp,  and,  there- 
fore, of  cessation  of  nutrition  of  the  dentine,  the  vital  relations  of  the 
cementum  and  alveolar  process  are  thus  maintained  and  the  useful- 
ness of  the  tooth  assured.  Whether  the  dentine  can  ever  receive 
nourishment  from  the  cementum  after  pulp  death  has  never  been 
scientifically  shown. 

Fig.  126. 


Portion  of  the  'side  of  a  root  of  a  tooth,  the  gum  and  alveolodental  membrane,  and  the  edge 
of  the  bone  of  the  alveolus.  A  band  of  fibres  is  seen  passing  over  the  surface  of  the  alveolus 
and  dividing,  some  passing  upward  into  the  gum,  others  passing  more  directly  across  to  the 
cementum.  Numerous  orifices  of  vessels  cut  across  transversely  are  seen  between  the  tooth 
and  the  bone.     (Black.) 


The  Pericementum.  {Syn.  Peridental  Membrane.)  The  peri- 
cementum is  the  highly  organized  remains  of  the  follicular  wall.  As 
the  alveolar  bone  and  cementum  develop  on  either  side  of  it,  it  forms 
also  the  periosteum  lining  the  alveolus.  It  is,  therefore,  the  means  by 
which  the  teeth  are  retained  in  their  sockets  and  a  certain  degree  of 
motion  permitted.  If  articulation  by  gomphosis  be  an  admissible 
term,  and  it  is  adopted  by  anatomists,  the  pericementum  subserves 
the  oflBce  of  a  ligament  not  altogether  unlike  that  found  in  the  sutures 
of  the  cranial  bones. 


DEVELOPMENT  OF  THE  TEETH. 


151 


It  is  continuous  with  the  periosteum  on  the  outside  of  the  alveolar 
process,  as  the  sutural  membrane  is  with  the  pericranial  membrane. 

Its  outline  study  divides  the  pericementum  into  three  portions — 
a  gingival,  an  alveolar,  and  an  apical  portion.^ 

It  is  composed  largely  of  white  fibrous  tissue  with  interlaced  blood- 
vessels, nerves,  and  glands.  It  also  contains  functional  cells,  fibro- 
blasts, cementoblasts,  osteoblasts,  and  osteoclasts. 

The  fibrous  tissue  is  made  up  of  principal  fibres  and  indifferent 
fibres.^ 


Fig.  127. 


^     ^ 


:;:— -  ->< 

?^  -  - 

«^  '  / 

/'■ 

/ 

i 

Longitudinal  section  of  the  peridental  membrane  in  the  gingival  portion:  D,  dentine;  [N, 
Nasmyth's  membrane;  C,  Cementum;  F,  fibres  supporting  the  gingivus;  F'^,  fibres  attached  to 
the  outer  layer  of  the  periosteum  over  the  alveolar  process;  F^,  fibres  attached  to  the  bone'at 
the  rim  of  the  alveolus;  B,  bone.     X  30  (about).     (Noyes.) 

The  principal  fibres  are  grouped  for  the  most  part  in  bands  or 
bundles  (Fig.  111). 

In  the  alveolar  portion  these  bundles  run  for  the  most  part  from 
the  cementum  to  a  higher  point  on  the  alveolar  process.  The  attach- 
ment is  secured  by  the  penetration  of  the  fibres  into  either  structure. 
This  secures  to  the  tooth  support  against  direct  pressure  into  the 
socket  and  against  rotary  motion. 


^  Noyes,  American  Text-book  of  Operative  Dentistry. 


2  n)id. 


152      ANATOMY  AXD  HISTOLOGY  OF  THE  JAWS  AXD  TEETH. 


At  the  apical  portion  the  l)an(ls  have  a  fan-hke  distribution.  In 
the  gingival  portion  the  fibres  are  directed  outward  and  sHghtly 
downward  for  attachment  to  the  process,  or  outward  and  downward 
over  the  edge  of  the  process  to  become  continuous  with  the  periosteal 
fibres,  or  outward  and  upward  with  the  submucous  gingival  tissue  to 
aid  in  the  support  of  the  gum  margin.  Some  of  the  gingival  fibres 
pass  from  the  cementum  of  one  tooth  to  that  of  the  next. 

The  bloodvessels  of  the  pericementum  are  derived  from  several 
sources:  (1)  from  several  vessels  derived  from  a  single  trunk  entering 
the  apical  space  from  the  bone  above;  (2)  from  vessels  entering  the 
membrane  through  the  Haversian  canals  of  the  alveolar  process  and 
anastomosing  with  branches  from  the  descending  arteries;  (3)  from 
the  vessels  of  the  outer  periosteum,  coming  over  the  edge  of  the  alve- 
olar process. 

There  are  comparatively  few  capillaries.  The  vessels  lie  mostly  in 
the  outer  or  alveolar  half  of  the  pericementum. 

This  disposition  of  the  arterial  blood  supply  ensures  nutrition  to 
the  peridental  membrane  in  case  of  loss  of  the  apical  tissue,  as  in  case 
of  apical  abscess,  and  also  ensures  a  collateral  blood  supply  to  the 

pulps  in  case  of  loss  of  main  arterial  trunks, 
as,  for  example,  in  operations  upon  the 
inferior  dental  canal. 

The  arteries  thus  furnishing  blood  to 
the  teeth  are,  for  the  upper  jaw:  the  an- 
terior dental  branch  of  the  infraorbital,  to 
the  upper  anterior  teeth ;  the  superior  den- 
tal branch  of  the  alveolar,  to  the  upper 
bicuspids  and  molars  and  the  bone  about 
their  root  ends;  the  descending  palatine 
and  its  anastomotic  connection,  the  spheno- 
palatine, supplied  to  the  palatine  side  of 
the  upper  alveolar  process,  etc. ;  the  alveo- 
lar, supplied  to  the  buccal  side  of  the 
upper  alveolar  process. 

In  the  lower  jaw  the  inferior  dental 
artery  and  its  incisor  branch  supply  the 
apical  tissues  of  the  lower  teeth  from  the  inferior  dental  canal.  Its 
mylohyoid  branch  supplies  the  gums  and  lingual  periosteum  of  the 
lower  alveolar  process,  the  mental  branch  supplies  the  lower  buccal 
process  anteriorly,  while  a  branch  of  the  facial  artery  anastomoses 


Fig.  128. 


Diagram  of  glands  of  peridental 
membrane.     (Black.) 


DEVELOPMENT  OF  THE  TEETH. 


153 


with  the  mental  anteriorly,  and  the  facial  sends  branches  to  the  cover- 
ings of  the  buccal  aspect  of  the  lower  jaw  posteriorly. 

The  veins  return  the  blood  by  similar  channels. 

The  nerves  of  the  pericementum  enter  by  several  trunks  in  the 
apical  tissue  and  also  enter  from  the  alveolar  wall  and  over  the  alveolar 
edge.  While  their  distribution  is  not  yet  fully  described,  some  of 
them  possess  the  tactile  sense,  as  touch  upon  the  teeth  is  fully  localized. 
They  are  derived  from  the  fifth  nerve  and  the  sympathetic. 


Fig.  129. 


Gnu 


Epithelial  structures:  Ee,  epithelial  oord,  apparently  showing  a  lumen;   Ch,  cementoblasts; 
Cm,  cementum;  D,  dentine.     X  500  (about).     (Noyes.) 


The  Pericemental  Glands.  Black  has  described  gland-like  structures 
lying  in  the  pericementum  nearer  the  cementum  than  the  alveolar  wall. 
These  are  distributed  over  the  root  in  a  network,  as  shown  in  Fig.  128. 

They  are  convoluted  cords  of  epithelial  cells  invested  with  a  delicate 
basement  membrane  and  can  be  traced  to  the  epithelium  of  the  gingival 
space,  but  not  to  the  surface. 

Traces  of  a  lumen  have  been  seen,  which  if  established  as  common 


Fig.  130. 


Longitudinal  section:  £p,  epithelium  lining  the  gingival  space:  Gj/,  gingival  gland,  so-called; 
D,  dentine;  N,  Nasmyth's  membrane;  Du,  duct-like  structure  stretching  away  toward  the  gin- 
givus  from  the  epithelial  cord,  seen  at  Ec ;  Cm,  cementum,  separated  from  the  dentine  by  decal- 
cification.    X  50  (about).     (Noyes.) 


DEVELOPMENT  OF  THE  TEETH  155 

would  constitute  them  as  tubes.  Their  function  is  not  definitely  known, 
but  it  is  presumptive  that  they  are  either  secreting  glands  or  lymphatics. 
The  entrance  of  bacteria  from  the  gingival  space  to  deep  portions  of 
the  pericementum,  there  to  develop,  may  possibly  be  favored  by  their 
presence  (Figs.  122  and  129). 

Glands  of  Series.  At  the  deepest  portion  of  the  gingival  space  is 
found  a  gland-like  body  which  has  been  given  the  above  name.  Its 
function  is  not  known  (Fig.  130,  Gg). 

The  Cellular  Elements.  The  fibroblasts  are  spindle-shaped  cells 
destined  to  become  mature  fibres.  They  lie  among  the  other  fibres. 
The  cementoblasts  lie  along  the  cementum  and  are  the  cementum 
builders.  Osteoblasts  are  found  engaged  in  bone  construction  along 
the  alveolar  wall.     (See  Figs.  64  and  65.) 

Osteoclasts,  large  multinucleated  cells,  lie  at  points  along  the 
cementum  of  teeth  and  alveolar  bone.  Their  office  is  the  removal  of 
bony  tissue.  They  remove  both  the  organic  and  inorganic  material, 
and  their  effects  are  seen  upon  the  cementum  and  dentine  of  the 
roots  of  teeth  undergoing  resorption,  also  upon  resorbed  alveolar 
process.  The  excavations  in  which  they  lie  at  work  are  called 
Howship's  lacunae. 

Calcospherites  are  sometimes  found  within  the  substance  of  the 
pericemental  membrane  and  may  have  some  significance  in  relation 
to  its  diseases. 

The  pericementum  in  the  young  is  comparatively  large  and  vascular, 
and  in  the  old  becomes  much  attenuated,  more  fibrous,  less  vascular, 
and  subject  to  degeneration. 

Union  of  alveolar  bone  and  cementum  but  rarely  occurs,  though  a 
mechanical  attachment  by  fibrous  pericementum  may  occur.  On  the 
other  hand,  the  union  of  the  cementum  of  one  tooth  with  that  of 
another  is  not  uncommon.     (See  Malformations  of  the  Teeth.) 


CHAPTER    VII. 

THE  SURGICAL  ANATOMY  OF  THE  TEETH. 

By  the  surgical  anatomy  of  the  teeth  is  meant  the  pecuhar  relation 
of  the  tissues  of  the  teeth  and  of  the  parts  immediately  adjacent  to 
diseases  arising  either  within  the  teeth  or  in  other  parts. 

THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY. 

Nasm3rth's  Membrane.  The  enamel  of  the  newly  erupted  tooth  is 
covered  by  Nasmyth's  membrane.  This  is  soon  worn  off  at  points 
exposed  to  wear,  persisting  longest  at  the  necks  and  in  the  fissures  of 
the  enamel,  in  which  situations  it  may  serve  as  a  breeding  ground  for 
micro-organisms. 

The  Enamel.  Enamel  once  formed  is  considered  to  have  lost  its 
source  of  nutrition  with  the  atrophy  of  the  ameloblasts  into  Nasmyth's 
membrane.  If  Caush  be  right,  it  is  possible  that  it  receives  nutrition 
via  the  enamel  tubes;  otherwise,  it  is  only  a  protective  covering  for 
the  dentine.  Its  resistance  to  acids  is  insuflScient  to  be  effective  if  the 
action  of  the  acid  be  concentrated  upon  it  for  a  time,  yet  it  is  much 
more  resistant  in  this  respect  than  dentine.  This,  however,  is  probably 
because  of  its  smoothness  and  homogeneity  of  structure. 

"If  two  blocks  of  equal  size,  one  of  enamel  and  one  of  dentine,  be 
subjected  to  stress,  it  is  seen  that  the  enamel  block  crushes  at  a  much 
lower  stress  than  that  of  dentine,  the  latter  being  elastic,  the  former 
inelastic;  this  appears  to  be  true  no  matter  in  what  axis  the  enamel 
is  pressed  upon;  but  if  a  layer  of  material  such  as  a  mat  of  soft  gold 
be  interposed  between  the  enamel  and  the  instrument  pressing  upon 
it,  its  resistance  is  much  increased."^  If  sections  of  the  crowns  of 
teeth  be  made,  it  will  be  seen  that  there  is  a  mechanical  arrangement 
of  the  enamel  elements  and  substances  fitted  to  counteract  the  innate 
brittleness  of  the  substance  itself.  First,  the  enamel  surfaces  are 
highly  polished,  so  that  there  is  a  minimum  of  friction  between  oppos- 
ing-teeth;  any  increase  of  roughness  or  any  jaggedness  of  enamel  robs 
the  teeth  of  this  advantage.     Secondly,  it  will  be  noticed  that  nearly 

1  Black. 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.        157 
Fig.  131. 


3tion  showing  carious  cavity,  secondary  dentine,  and  pulp  nodules  by  ordinary  transmitted 

illumination.      (Kirk.) 

Fig.  132. 


Same  as  Fig.  131,  showing  greater  transparency  of  highly  calcified  structures  by  polarized 

light.      (Kirk.) 


158  THE  SURGICAL  ANATOMY  OF  THE  TEETH. 

all  of  the  enamel  surfaces  which  are  brought  into  action  during  masti- 
cation receive  mechanical  support  through  an  appropriate  arrange- 
ment of  enamel  masses. 

Its  attachment  to  the  dentine  is  greatest  in  vital  teeth,  owing  probably 
to  the  integrity  of  the  dentinal  tissue  at  the  point  of  attachment; 
nevertheless  the  attachment  is  considerable  in  even  devitalized  teeth. 

The  arrangement  of  the  enamel  rods  is  such  as  to  afford  the  greatest 
possible  resistance  to  stress. 

The  Dentine.  Dentine  is  the  second  hardest  tissue  of  the  body.  The 
texture  of  this  tissue  changes,  as  does  that  of  the  other  connective 
tissues,  with  age.  In  the  young  or  immature  dentine  there  is  a  greater 
ratio  of  organic  matter  than  in  the  dentine  of  a  middle-aged  person- 
The  increase  of  calcium  salts,  the  inorganic  constituents,  has  been 
shown  by  Black  not  to  be  so  great  as  was  formerly  believed.  The 
average  amount  of  calcium  salts  in  teeth  at  the  age  of  11  years  is 
found  to  be  62.26  per  cent.;  at  53  years  the  percentage  is  64.56.  The 
average  specific  gravity  at  11  years  is  1.066,  and  at  63  years  2.109. 
While  in  the  main  the  increase  of  specific  gravity  corresponds  with  the 
increase  of  calcium  salts,  it  is  not  constant.  Between  the  ages  of 
twenty  and  forty  years  there  appears  to  be  a  cessation  in  the  increase 
of  calcium  salts. 

These  facts  show  that  increase  of  density  is  caused  by  deposition  of 
dentinal  substance  rather  than  a  mere  increase  of  calcium  salts. 
(See  Transparency  of  Dentine.) 

Dentine  is  an  elastic  substance:  a  cube  of  -j^j^  inch  side  under  a 
stress  of  150  pounds  is  compressed  4  per  cent,  of  its  thickness,  resum- 
ing its  form  after  removal  of  the  pressure.  Under  a  pressure  of  238 
pounds  the  cube  is  crushed.  Clear  and  translucent  dentine  has  a  high 
crushing  stress;  in  opaque  specimens  it  is  much  lower.  An  increase  in 
the  percentage  of  calcium  salts  diminishes  the  elasticity  of  dentine;  but 
the  amount  of  crushing  stress  appears  to  be  governed  more  by  the  con- 
dition of  the  organic  matrix  than  by  the  percentage  of  calcium  salts  or 
the  density.  When  the  nutrition  of  the  dentine  is  interfered  with  by 
secondary  deposits,  or  destroyed  through  death  of  the  dental  pulp,  the 
dentine  appears  to  diminish  in  strength,  as  seen  in  the  abraded  teeth 
of  elderly  persons. 

The  average  percentage  of  organic  matter  in  dentine  is  25.36;  this 
diminishes  as  the  density  increases.  Black  believes  that  the  condition 
of  the  organic  matrix  of  the  teeth  has  more  to  do  with  the  strength  of 
the  teeth  than  have  the  density  and  specific  gravity.    The  proportion 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY 


159 


of  organic  matter,  as  pointed  cut  by  Miller,  is  not  an  exact  measure  of 
the  hardness  of  the  dentine,  for  many  interglobular  spaces  and  wide 


Fig.  133. 


Enamel  and  dentine  of  deciduous  molar.     (Kirk.) 
Fig.  134. 


Same  as  Fig.  133,  photographed  by  polarized  light.      (Kirk.) 


160  THE  SURGICAL  AS  ATOMY  OF  Till-:  TEETH. 

tubules  may  account  for  a  hi*i;li  percentatje  of  ()i(>anic  matter,  and  yet 
the  dentine  of  the  tooth  be  very  dense. 

Black's  researches  showed  that  there  is  a  greater  variation  in  the 
density  and  specific  gravity  of  the  individual  teeth  of  a  denture  than  is 
found  in  the  general  average  density  of  many  persons. 

Investigations  conducted  by  Kirk'  with  polarizefl  light,  to  determine 
possible  variations  in  the  degree  of  density  or  calcification  of  the 
various  structures  composing  the  teeth,  show  that  such  variations 
exist,  not  only  in  different  teeth,  but  in  the  same  tooth  and  the  same 
tissue  of  the  tooth,  and  even  within  what  are  apparently  normal 
tissues.  The  variations  probably  represent  the  nature  and  degree  of 
calcification  or  possible  alterations  as  the  result  of  sclerotic  change. 

The  dentine  presents  for  consideration  several  structures  of  surgical 
interest : 

1.  The  subenamel  dentine. 

2.  The  body  of  the  dentine  containing  tubules  and  intertubular 
substance. 

3.  The  protoplasmic  material  in  the  tubules. 

4.  Accidental  malformations,  such  as  interglobular  spaces. 

5.  The  pulp  cavities. 

That  portion  of  dentine  just  beneath  the  enamel  seems  more  subject 
to  the  action  of  the  causes  of  caries  than  the  more  typical  dentine,  so 
that  once  accesss  is  gained  to  it  the  micro-organisms  spread  readily 
along  this  tissue.  The  decussations  of  the  tubules,  however,  may 
assist  in  this  process. 

Sections  of  teeth  which  have  been  subjected  to  the  prolonged  action 
of  dilute  acids  show  that  the  dentine  immediately  surrounding  the 
protoplasmic  filaments  from  the  odontoblasts  is  more  resistant  to  the 
action  of  the  acids  than  the  formed  material  of  the  dentine.  Noting 
this  comparative  insolubility,  this  portion  of  the  dentine  (Neumann's 
sheaths)  has  been  accepted  as  a  partially  calcified  tissue. 

There  seems  to  be  no  rational  foundation  for  the  contention  of  the 
Heitzmann  school  of  histologists  that  the  basis  substance  of  dentine 
undergoes  retrograde  metamorphosis  or  return  to  the  embryonic  con- 
dition during  dental  caries,  Miller  having  shown  that  the  embryonal 
elements  are  in  reality  micro-organisms,  or  that  resorption  and  re- 
depositions  occur  during  pregnancy.  Black's  analyses  indicate  that 
no  such  resorption  and  deposition  occur. 

1  Dsntal  Cosmos,  May,  1903. 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.        161 

The  dentinal  fibril  is  the  occupant  of  the  lumen  of  the  tubule. 
These  tubules  afford  avenues  by  which  the  fungi  of  caries  gain  deep 
access  to  the  dentine,  and  working  from  which  sites  they  readily  destroy 
the  tubule  wall  and  intertubular  substances.  During  the  process  the 
fibrillae  have  their  function  at  first  exalted  and  are  then  destroyed  for 
a  distance.  The  exaltation  of  function  causes  some  vital  manifestations 
capable  of  interpretation  as  a  resistance  to  the  progress  of  caries, 
abrasion,  or  erosion.  (See  Hypersensitivity  of  Dentine,  Tubular  Cal- 
cification, Secondary  Dentine). 

Interglobular  spaces  existing  in  the  dentine  contain  an  uncalcified 
material  through  which  the  tubules  pass  uninterruptedly.  The  fungi 
of  caries  obtaining  access  to  them  via  the  tubules,  etc.,  multiply  readily 
at  the  expense  of  their  contents,  the  process  of  caries  being  thereby 
accelerated. 

The  uncovering  of  the  dentine  from  any  cause  exposes  its  fibrillae, 
which,  being  acted  upon  by  external  agencies,  may  become  hyper- 
sesthetic,  producing  the  phenomenon  of  hypersensitive  dentine. 

The  Pulp  and  the  Pulp  Cavities.  The  pulp  occupies  the  pulp 
chamber  of  the  crown,  and  one  radicular  portion  runs  into  each  root 
canal.  It  conforms  in  regularity  to  the  outline  of  the  pulp  cavity  or 
cavities  and  extends  through  the  apical  foramen  or  foramina,  to  be 
fused  with  the  tissue  of  the  apical  space  from  which  it  derives  its 
vascular  and  neural  supply. 

Beneath  each  cusp  or  incisal  angle  of  the  crown  it  has  fine  pro- 
jections called  cornua  (horns),  which  render  exposure  by  caries  or 
excavation  liable  to  first  occur  at  that  point.  It  is  attached  to  the 
dentine  by  means  of  its  odontoblastic  prolongations — the  fibrillse.  In 
a  general  way  its  form  is  a  miniature  of  the  external  form  of  the  tooth, 
but  differences  in  relative  length  of  cornua  occur  (Fig.  138). 

The  vascular  network  of  the  pulp  is  in  close  relation  to  the  odonto- 
blasts, and  nerves  have  been  traced  to  endings  between  them,  though 
as  yet  no  nerve  fibrils  ending  in  the  odontoblasts  have  been  discovered. 
The  attenuation  of  the  muscular  coats  of  the  vessels  has  a  direct 
relation  to  the  hypersemic  diseases  of  the  pulp.  The  lack  of  tactile 
nerve  endings  in  the  pulp  accounts  for  the  reflected  character  of  its 
pains. 

The  constriction  of  the  pulp  at  the  apex  renders  its  arteries  and  veins 
liable  to  mutual  compression  during  hypersemia,  and  the  relations  of 
the  pulp  with  the  apical  tissue  render  liable  the  involvement  of  one 
in  disease  of  the  other.    The  pulp  decreases  in  size  with  age  and  under 

11 


162 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


stimulus  of  certain  dental  diseases  in  exact  ratio  with  the  diminution 
in  size  of  the  pulp  cavity. 

It  also  at  times  forms  within  itself  hard  bodies  known  in  a  general 
way  as  pulp  nodules. 


Fig.  135. 


Fig.  136. 


Fig.  137. 


Fig.  138. 


Fig.  140. 


Fig.  142. 


Longitudinal  and  transverse  sections  of  upper  teeth,  showing  shapes  of  pulp  chambers  and 

their  positions. 

The  general  forms  of  the  pulp  cavities  may  be  studied  in:  (1)  longi- 
tudinal and  transverse  sections  of  extracted  teeth;  (2)  by  direct  and 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.      163 

tactile  observation  of  such  teeth  in  the  mouth  during  the  course  of 
treatment;  (3)  by  skiagraphs  of  teeth  in  situ,  and  (4)  by  the  use  of 
formahn  gelatin  injected  into  pulp  canals  of  extracted  teeth.  After 
hardening  the  tooth  is  itself  digested  away,  leaving  the  formalin  gelatin 
as  a  cast  of  the  canal  interior  (Figs.  151  and  152). 


Fig.  143. 


Fig.  144. 


Fig.  145. 


Longitudinal  and  transverse  sections  of  lower  teeth,  showing  shapes  of  pulp  chambers  and 

their  positions. 


The  form  and  location  of  pulp  cavities  are  of  importance  in  con- 
sidering the  depth  of  possible  excavation  of  cavities,  the  exposure  of 
pulps  by  caries,  the  formation  of  secondary  dentine,  and  the  necessary 
treatment  of  pulps  and  of  pulp  canals  in  the  therapeutics  of  diseases 
of  the  pulp  and  pericementum. 

Cementum  and  Pericementum.  At  the  apex  of  the  root  the  pulp 
is  continuous  with  the  structures  external  to  the  tooth,  viz.,  the 
pericementum. 


164 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


Formalin-gelatin  casts  of  pulp  ca\aties,  showing  pulp  irregularities.      (Richards.)l 

Fig.  152. 


Formalin-gelatin  casts  of  pulp  cavities  compared  with  the  teeth  themselves.     (Richards.) 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.        165. 

The  pericementum  is  the  touch  organ  of  the  tooth,  the  nerves 
possessing  the  sense  of  location.  The  pericementum  is  the  mutual 
periosteum  of  the  cementum  of  the  tooth  and  of  the  enclosing  alveolar 
wall;  reflected  over  the  external  alveolar  wall  this  periosteum  becomes 
continuous  with  the  general  maxillary  periosteum.  In  addition,  the 
pericementum  is  the  ligament  binding  the  tooth  in  its  articular  (the 
alveolar)  walls.  As  a  periosteum  it  is  a  source  of  nutrition  to  the 
cementum  and  to  portions  of  the  alveolar  walls,  so  that  interference 
with  its  vascular  supply  is  followed  by  malnutrition  of  these  tissues, 
the  effects  being  governed  by  the  extent  of  the  interference.  (See  Gen- 
eral Pathology).  As  a  ligamentous  tissue,  its  fibres,  as  shown  by  Black, 
have  a  peculiar  arrangement.  The  bundles  of  fibrous  connective  tissue 
which  pass  from  the  alveolar  walls  to  the  cementum  are  oblique  in  their 
general  direction,  the  fibres  passing  from  a  point  nearer  the  margin  of 
the  alveolus  to  a  deeper  portion  of  the  root. 

The  nerves  of  the  pericementum  are  accustomed  to  a  degree  of 
pressure  represented  in  the  amount  of  force  necessary  to  crush  the 
particles  of  food;  if  subjected  to  a  greater  stress,  they  rebel.  Similarly, 
if  their  functional  activity  is  exalted  in  hypersemic  disturbances,  they 
become  cognizant  of  very  slight  pressure  and  react  more  strongly.  It 
is  to  be  remembered,  however,  that  the  teeth  rarely  receive  direct  stress, 
the  movements  of  the  teeth  in  mastication  being  more  of  a  rotary  and 
laterally  moving  character,  than  perpendicular. 

The  elasticity  of  the  pericementum  is  to  be  regarded  also  as  an 
adjuvant  to  the  local  circulation;  by  its  movements  the  blood  is  pumped 
through  the  vessels  of  the  part.  This  fact  becomes  important  when  it 
is  recognized  that  in  some  dentures  increasing  age  is  accompanied  by 
a  lessening  of  the  volume  and  elasticity  of  the  pericementum. 

The  power  of  recovery  of  the  pericementum  after  injury  appears  to 
be  very  great.  It  will  be  observed  that  the  pericementum  has  two 
sources  of  vascularity :  one  from  the  apical  vessels,  that  from  which  the 
vascular  supply  of  the  pulp  arises;  the  other,  an  anastomotic  circulation 
from  the  alveolar  walls,  directly  and  indirectly  from  the  general 
alveolar  periosteum.  When  the  apical  vessel  trunks  have  been  obliter- 
ated as  the  result  of  disease  the  pericementum  receives  from  the  anasto- 
motic circulation  a  blood  supply  practically  sufficient. 

The  cementum  maintains  its  vitality  so  long  as  the  pericementum  is 
intact;  in  the  condition  just  mentioned  it  is  evident  that  the  apical 
portion  of  the  cementum  dies,  or  is  at  best  very  ill-nourished.  The 
layer  of  cementoblasts  (osteogenetic  cells)  retain  their  function  so  long 


166 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


as  the  pericementum  is  intact,  and  under  varied  conditions  exert  their 

constructive  function  in  an  irregular  manner.    (See  Hypercementosis.) 

The  Teeth  as  Mechanical  Appliances.     Architecturally  the  upper 

incisors  and   cuspids  are  protected    against  an  outward   strain  from 


Fig.  153. 


Architectural  structure  of  an  incisor. 


Architectural  structure  of  a  cuspid. 


the  antagonizing  lower  teeth,  tending  to  break  away  the  labial  section 
of  the  teeth  (Fig.  153,  bd)  by  buttresses  (Fig.  153,  b,  b)  and  a  cervical 
girdle  (Fig.   153,  g),  and  are  further  fortified  by  labial  stanchions 

(Figs.  153  and  154,  s  s  s). 


Fig.  155. 


Fig.  156. 


Fig.  157. 


Architectural  elements  of  bicuspids  and  molars. 

The  bicuspids  and  molars  receiving  the  cusps  of  antagonizing  teeth 
into  their  sulci,  which  are,  architecturally  speaking,  points  of  weakness, 
have  a  tendency  to  split  between  the  cusps,  which  are  strengthened 
by  girders  (Figs.  155,  156  and  157,  g). 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.       167 


Decay  destroying  any  of  these  points  weakens  the  teeth,  but  up 
to  a  certain  point  loss  of  tissue  is  not  fatal  to  the  integrity  of  the  tooth, 
as  shown  by  its  behavior,  both  before  and  after  filling  for  dental  caries. 

An  excessive  loss  of  dentine,  however,  is  apt  to  be  followed  by  fracture 
when  an  undue  strain  is  applied.  The  dentine  of  devitalized  teeth 
has  less  cohesion  than  vital  dentine,  but  in  otherwise  sound  teeth  it 
is  sufficient  for  ordinary  use. 


Fig.  158. 


Fig.  159. 


The  rotary  movements  of  the  lower  jaw  bring  about  between  the 
teeth  a  gliding  movement  of  their  articular  surfaces  rather  than  a 
direct  impact,  which,  however,  may  be  imparted  in  the  effort  to  crush 
hard  bodies. 

In  the  lower  anterior  teeth  labio  lingual  stress  exerted  by  the  upper 
teeth  forces  the  teeth  together  laterally,  affording  mutual  support 
(Fig.  158). 

Fig.  160. 


The  lower  ja-w  as  a  lever  of  the  third  class. 

The  upper  anterior  teeth  enclosing  the  lower  anterior  teeth  prevents 
outward  displacement  of  the  latter  by  the  force  of  the  tongue.  The 
upper  posterior  teeth  are  inclined  outward,  the  lower  posterior  teeth 
inward,  an  arrangement  best  suited  to  resist  the  mutual  pressure 
exerted  in  mastication. 


168 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


The  enamel  dentine  and  cementum,  if  exposed,  are  subject  to  the 
action  of  abrasion,  erosion,  and  caries  (which  see). 

The  Alveolar  Process.  The  alveolar  process  is  that  portion  of  bone 
which  is  continuous  with  the  body  of  the  maxilla,  and  is  built  up  as 
a  support  to  the  teeth.  In  general  it  differs  but  little  from  the  bone 
of  the  jaw,  consisting  internally  of  cancellated  bone  bounded  by  more 
dense  bone  externally.    The  surface  of  bone  lining  the  alveoli  is  also 


Fig.  161. 


Showing  the  buccal  surfaces  of  the  crowns  and  roots  in  position.     (Cryer.) 

fairly  dense,  being,  however,  pierced  by  many  spaces  affording  passage 
of  vessels  to  the  pericementum.  The  openings  in  the  cancellated  bone 
contain  red  bone-marrow.  The  walls  of  the  alveoli  afford  attachment 
to  the  pericementum,  which  thus  becomes  its  periosteum.  The  division 
of  the  pericementum  into  an  alveolar  and  cemental  membrane  having 
different  functions  is  not  regarded  favorably  by  Tomes,  though  claimed 
by  some  histologists. 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.        169 

The  relations  of  the  teeth  and  alveolar  process  are  further  shown 
by  Figs.  162  and  168. 

Under  the  action  of  chronic  inflammation  the  cancellated  bone 


Fig.  162. 


Vertical  section  of  a  frozen  head,  rear  view.  Shows  relations  of  roots  of  molars  and  the 
maxillary  sinus,  and  of  the  maxillary  sinus  with  the  frontal  sinus.  Wire  passes  from  the  latter 
through  the  infundibulum,  the  hiatus  semilunaris,  and  the  ostium  maxiilare,  into  the  maxillary 
sinus,  establishing  a  connection.      (Cryer.) 


170 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


may  undergo  a  constructive  chano-e  (condensing  osteitis),  and  is  more 
firmly  bound  to  the  cortical  bone.  Cryer  has  shown  that  this  may 
prevent  the  forward  movement  of  the  cancellated  bone  and  thus  prevent 
the  proper  placement  of  teeth  in  the  jaw.  He  regards  this  as  a  cause 
of  impaction. 

The  anatomy  and  histology  of  the  teeth  and  immediate  surroundings 
have  a  direct  relation  to  the  consideration  of  the  pathology  and  surgical 
treatment  of  diseases  of  the  parts. 

The  length,  size,  number,  and  form  of  roots  bear  a  direct  relation 
to  the  security  of  implantation,  a  consideration  of  importance  in  view 


Fig.  163. 


Oins 


0ms 


1st  M  1st  31 

Section  of  somewhat  dried  specimen:  0ms,  opening  maxillary  sinus;   1st  M,  first  molar. 

(Cryer.) 

of  the  strains  to  be  brought  to  bear  upon  prosthetic  appliances,  such 
as  crowns,  bridges  or  plates,  or  upon  remaining  natural  teeth.  In  the 
determination  of  such  conditions  a;-ray  skiagraphs  are  valuable. 

The  Lower  Denture.  Reference  to  Fig.  164  will  show  the  relation 
of  the  roots  of  the  lower  incisors  and  cuspids  to  the  alveolar  process 
and  jaw.  The  apices  of  the  roots  lie  at  a  point  below  the  reflection 
of  the  mucous  membrane.  Labially  the  bone  is  thick  over  their  apices 
and  at  their  necks,  and  sometimes  thin  at  the  middle  portion;  lingually 
the  bone  is  thickest  over  the  apices.  Apical  abscesses  tend  to  discharge 
labially,  following  a  course  from  the  apex  to  a  point  above  the  mucous 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY. 


171 


Fig.  164. 


reflection.  They  sometimes  discharge  hngually.  They  may  follow 
the  cancellated  bone  and  penetrate  the  cortical  layer  at  the  rim  of 
the  jaw  and  discharge  through  the 
soft  tissues  upon  the  chin.  Again, 
penetrating  the  cortical  bone  labi- 
ally,  they  may  dissect  away  the  peri- 
osteum of  the  bone  and,  reaching 
the  rim  of  the  jaw,  discharge  through 
the  soft  tissue  upon  the  chin.  (See 
Chronic  Apical  Abscess.) 

The  bone  overlying  the  roots  of  the 
lower  bicuspids  at  their  lingual  as- 
pects is  sometimes  relatively  thin,  as 
it  forms  the  wall  of  the  sublingual 
fossa.  Upon  the  buccal  face  the 
cortical  bone  is  in  greater  amount, 
although  thin.  The  spaces  between 
the  first  and  second  bicuspids  usu- 
ally mark  a  site  immediately  above 

.1  ,    1      p  1,1  1       ji  a  longitudinal  section  through  a  lower  cen- 

the   mental   foramen,    although    the       ^.^i  -^^^-^^^  ^^^  -^^^  neighboring  parts. 


Fig.  165. 


From  the  same  jaw  as  Fig.  161,  showing  outline  of  inferior  dental  canal  and  the  surrounding 
cancellated  bone.     (Cryer.) 


opening  may  be  posterior,  or  in  some  cases  anterior,  to   the  position 
named    (Fig.    165).      If   the  roots  of  the  bicuspids  are  abnormally 


172 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


Fig.  166. 


long,  they  may  encroach  npon  the  area  of  the  foramen.  This  occurs 
most  frequently  with  the  root  of  the  second  bicuspid,  affections  of 
which  tooth  may  cause  diffused  pain,  apparently  owing  to  the  prox- 
imity of  the  root  apex  to  the  nerve  trunk  at  the  foramen. 

Reference  to  Fig.  166  will  show  the  relation  of  lower  molars  to  the 
body  of  the  bone,  the  alveolar  process,  the  inferior  dental  canal,  and 
the  submaxillary  triangle. 

The  root  of  the  third  lower  molar  may  terminate  at  a  point  some 
distance  behind  the  anterior  pillar  of  the  fauces.  Upon  the  external 
or  buccal  face  of  the  bone  it  will  be  seen  that  the  position  of  the  third 

molar  is  at  times  some  distance 
posterior  to  the  outer  branch  of  the 
base  of  the  coronoid  process,  the 
continuation  of  the  external  oblique 
line,  so  that  a  greater  distance  sepa- 
rates the  roots  of  the  second  and 
third  molars  from  the  external  sur- 
face of  the  bone  than  with  any  of  the 
teeth  of  a  denture.  Abscess  upon 
the  roots  of  particularly  the  lower 
third  molar,  therefore,  finds  the 
path  of  least  resistance  as  to  pus 
exit,  first,  by  destroying  the  perice- 
mentum of  the  tooth  and  finding 
exit  at  the  gum  margin,  or,  if  the 
outer  alveolar  plate  be  not  entirely 
walled  in  by  the  base  of  the  coro- 
noid process,  through  the  alveolar 
process  near  the  gum  margin.  An 
abscess  may,  by  penetrating  the 
lingual  alveolar  wall,  open  far  back 
in  the  mouth,  if  the  roots  of  the 
tooth  are  not  deeper  than  the  mylo- 
hyoid ridge;  if  the  roots  do  pene- 
trate beyond  this  ridge,  it  may  open  in  the  neck  in  the  submaxillary 
triangle. 

In  some  cases  the  roots  of  the  second  and  third  molars  may  immedi- 
ately overlie  the  inferior  dental  canal,  and  the  tissue  intervening  between 
the  apices  of  the  molar  roots  and  the  canal  may  consist  of  the  very  thin 
layer  of  perforated  cortical  bone  which  forms  the  roof  of  the  canal. 


Showing  the  relations  of  the  roots  of  the 
lower  third  molar  with  the  cavities  of  the 
mouth  and  neck,  and  with  the  external  bony 
wall:  ^4,  cavity  of  mouth  separated  from  B, 
the  caAdty  of  the  neck,  by  the  mylohyoid 
muscles;  C,  base  of  coronoid  process;  D, 
muscles  of  the  cheek. 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY.       173 

In  some  cases  a  molar  root  may  be  so  deeply  embedded  as  to  encroach 
upon  the  canal,  lessening  its  lumen  and  causing  more  or  less  compression 
of  the  inferior  dental  vessels  and  nerves  (Fig.  240).  Pressure  from 
such  sources  is,  no  doubt,  the  cause  of  obstinate  maxillary  neuralgias, 
which  would  be  greatly  exaggerated  in  disease  conditions  about  the 
pericementum,  accompanied  by  inflammation  or  even  hypersemia.  In 
impacted  third  molars  the  pressure  of  some  part  of  the  tooth  may 
cause  great  distortion  of  the  course  of  the  canal.  The  anatomical 
relations  of  the  third  lower  molars  are  such  that  apical  abscess  upon 
them  will  have  tardy  vent,  or  else  open  in  unusual  situation. 

The  blood  supply  to  the  inferior  maxilla  through  the  inferior  dental 
artery — large  single  trunks  which  traverse  the  bone  longitudinally  upon 
both  sides — may  be  seriously  impeded  or  checked  by  pressure  upon  the 
trunk  as  it  enters  or  shortly  after  its  entry  to  the  canal,  and  thus 
necrosis  of  half  the  maxilla  is  a  probable  danger.  In  many  cases, 
however,  where  the  inferior  dental  vessels  have  been  obliterated  by 
operation  upon  one  side  necrosis  does  not  occur,  the  anastomosis  of 
the  facial  artery  with  the  dental  about  the  mental  foramen  continuing 
sufficient  circulation  to  maintain  vitality. 

The  Upper  Denture.  In  the  upper  jaw  the  inner  alveolar  plate  is 
thicker  than  the  outer,  particularly  when  the  vault  is  low.  In  general 
terms,  the  higher  the  arch  of  the  vault  the  thinner  the  inner  alveolar 
plate.     (Compare  Figs.  162  and  163.) 

The  central  incisor  lies  beneath  the  nasal  cavity  with  its  root  end  on 
a  level  with  the  lowest  portion  of  the  nasal  spine.  It  is  in  somewhat 
close  relation  with  the  anterior  palatine  canal.  The  lateral  incisor  also 
underlies  the  nasal  cavity  at  the  ala  nasi ;  its  root  end  is  one-eighth  inch 
less  implanted,  though  sometimes  more  deeply.  The  cuspid  root  lies 
with  its  apex  implanted  one-eighth  inch  deeper  than  that  of  the  central. 
It  is  not  under  the  antrum,  but  slightly  anterior  to  it.  In  occasional 
instances  it  may  underlie  the  lower  anterior  portion  of  the  antrum. 

Any  of  the  upper  bicuspids  or  molars  may  underlie  the  antrum, 
but  intimate  association  of  the  root  apices  with  its  floor  is  usual  only 
with  the  second  bicuspid  and  the  molars  (Fig.  167).  The  apices  of 
the  roots  of  the  latter  may,  in  abnormal  skulls,  lie  directly  in  the 
antrum  and  be  covered  only  by  the  periosteum  and  mucous  membrane. 
In  other  cases  the  bone  is  thinly  distributed  over  them. 

The  antrum  enlarges  with  age,^  and  the  resorption  may  produce  the 
same  effect. 

^  Oyer. 


174 


THE  SURGICAL  ANATOMY  OF  THE  TEETH. 


Fig.  167. 


It  is  clear  that  alveolodental  abscess  may  readily  discharge  in  this 
situation  into  the  sinus,  or  that  fractures  of  the  floor  of  the  antrum 
may  occur  in  extractions,  either  by  crushing  in  or  tearing  out  portions 
interlocked  with  roots.    The  elevation  produced  by  the  malar  process 

overlies  the  roots  of  the  first  molar. 
The  roots  of  the  upper  third  molar  lie 
in  the  tuberosity  of  the  upper  maxilla 
and  in  close  relation  to  the  descending 
palatine  artery.  It  has  been  pushed  into 
the  antrum  in  attempt  at  extraction,  and 
its  extraction  has  also  resulted  in  frac- 
ture of  this  tuberosity,  exposing  the 
antrum. 

It  is  pointed  out  by  Cryer  that  the 
frontal  sinuses  may  communicate  with 
the  maxillary  sinus.  Fig.  162  shows  a  wire  passing  from  the  left 
frontal  sinus  to  the  antrum  via  the  infundibulum,  hiatus  semilunaris, 
and  ostium  maxillare.  The  possibility  of  relation  of  these  sinuses 
in  disease  is  plainly  shown. 

Fig.  168. 


Outline  of  antrum,    (s^kiagraph  by 
Custer.) 


Front  and  side  views  of  the  teeth  and  jaws. 


The  Occlusion  of  the  Teeth.  Viewed  in  occlusion — that  is,  with 
all  the  teeth  together  and  at  rest — the  teeth  present  the  relation  shown 
in  Fig.  168,  in  which  it  may  be  seen  that  the  occluded  surfaces  of  the 
upper  teeth  describe  a  curve  with  the  convexity  slightly  downward. 

The  lower  teeth  have  the  reverse  curve. 


THE  TISSUES  OF  THE  TEETH  VIEWED  SURGICALLY 


175 


Fig.  169. 


The  longer  the  cusps  of  the  teeth — i.  e.,  the  greater  the  overbite — the 
greater  the  curve  of  the  arch  will  be. 

The  Articulation  of  the  Teeth.  The  lower  jaw  is  a  lever  of  the 
third  class,  the  fulcrum  being  the  condyles,  the  weight  the  work  done 
by  the  teeth,  and  the  power  applied  at  an  intermediate  point 
by  the  temporal  muscles  at  the  coronoid  process,  the  masseter 
muscles  at  the  ramus  and  angle  of  the  jaw  (Fig.  160).  These  produce 
the  closing  or  occluding  power  of  the  jaw  (occlusion).  The  internal 
pterygoid  muscle  attached  at  the  inner  surface  of  the  angle  draws  the 
jaw  sidewise  to  the  side  opposite  that  upon  which  the  muscle  is  con- 
tracting. The  two  heads  of  the  external  pterygoid  attached  at  the 
condyle  project  the  jaw  forward. 

This  combined  action  imparts  to  the  lower  jaw  a  forward,  sidewdse, 
and  occluding  movement  which  causes  the  teeth  to  glide  over  each 
other,  the  jaws  being  slightly  opened  as  the  articu- 
lar surfaces  of  the  molar  cusps  come  into  contact. 
This  movement  is  called  articulation. 

Suppose  Fig.  169  to  represent  an  anterior  view 
of  an  upper  and  lower  right  molar.  As  the  lower 
jaw  is  thrust  to  the  right  the  jaw  slightly  opens, 
the  buccal  cusp  of  the  lower  molar  leaves  its  point 
of  occlusion  in  the  sulcus  of  the  upper  molar,  and 
presents  its  articulating  surface,  D,  to  that  of  the 
buccal  cusp  of  the  upper  molar,  A.  At  the  same  time 
F  glides  over  C.  In  the  reverse  motion  the  buccal 
cusp  of  the  lower  molar  is  returned  to  the  sulcus, 
and  then  E  glides  over  B,  C,  and  F,  meanwhile 
separating.  In  normally  articulating  molars  G  and 
H  are  unworn.  In  the  bicuspids  the  articulation  of  C  with  F  does  not 
occur  except  to  a  very  limited  degree  between  the  lower  first  molar 
and  upper  second  bicuspid. 

The  lower  incisors  and  cuspids  articulate  only  upon  their  lablo- 
incisal  edges,  while  the  upper  incisors  and  cuspids  articulate  with 
their  lingual  surfaces  and  linguo-incisal  edges,  the  articulation  begin- 
ning at  the  linguo-incisal  margin  (with  the  jaws  opened  and  lower  jaw 
thrust  forward)  and  gliding  cervically  as  the  jaw  closes  and  recedes 
until  the  molars  are  in  contact.  In  the  lateral  motion  of  the  jaws  some 
teeth  are  in  articulation  on  both  sides,  and  the  cuspids  on  one  side 
or  the  other  are  in  contact.  They  seem,  therefore,  to  act  as  guides 
in  articulation. 


Diagram  illustrating 
articulation. 


176  THE  SURGICAL  AX  ATOMY  OF  THE  TEETH. 

The  abnormal  occlusion  and  articulation  of  the  teeth  are  consequent 
upon  the  eruption  of  the  teeth  into  irregular  situations,  or  upon  inju- 
dicious extractions,  or  upon  diseases  or  habits  leading  them  into 
abnormal  relations  with  their  antagonists.  (See  Abrasion,  Mal- 
positions, etc.) 

Black^  found  by  test  that  the  force  which  the  muscles  of  mastication 
of  adults  were  capable  of  exerting  was  from  30  to  175  pounds  on  the 
incisors,  and  from  70  to  240  pounds  on  the  molars.  The  figures  repre- 
sent the  minimum  and  maximum  total  capacity  found.  The  temporary 
molars  averaged  about  70  pounds.  The  amount  of  force  required  to 
crush  foodstuffs  by  direct  action  ranges  from  30  pounds  for  tender 
meats  to  90  pounds  for  tough,  fried  meats;  100  pounds  for  hard  candy, 
and  250  pounds  for  hard  crusts. 

Black  states  that  many  persons  fail  to  exert  the  muscles  to  their 
full  capacity  owing  to  the  debility  of  the  pericementum  of  one  or  more 
teeth. 

Diagnosis  of  Teeth.  At  a  time  when  both  temporary  and  per- 
manent teeth  are  in  the  mouth  they  must  often  be  carefully  distin- 
guished. 

Their  greater  size  and  deeper  color,  as  well  as  form  and  position 
in  the  mouth,  characterize  the  permanent  teeth.  The  temporary  teeth 
have  an  abrupt  shoulder  of  enamel  at  the  cervix  not  present  in  the 
permanent  teeth. 

1  Dental  Cosmos,  June,  1895. 


CHAPTER   VIII. 

DENTITION :  ITS  PROGRESS,  VARIATIONS,  AND  ATTENDANT 

DISORDERS. 

The  process  of  teething,  eruption,  or  dentition  is  comprised  of  that 
series  of  vital  operations  which  causes  the  teeth  to  leave  their  cr}^ts 
in  the  maxillae,  to  pierce  the  gum,  and  to  take  their  places  in  the 
dental  arches.  It  is  a  continuation  of  the  process  of  dental  develop- 
ment and  is  accompanied  and  succeeded  by  root,  alveolar,  and  max- 
illary developments,  which  are  also  to  be  considered  in  connection- 
with  it. 

Physiologically  dentition  is  divided  into:  (1)  the  first  dentition  or' 
that  of  the  temporary  teeth;  (2)  the  second  dentition  or  that  of  the 
permanent  teeth. 

Examination  of  Fig.  96  will  show  the  state  of  tooth  development 
at  a  period  shortly  after  birth  (a  central  incisor  being  under  con- 
sideration). The  crypt  is  roofed  over  at  birth  by  a  membranous 
structure.  During  the  period  from  then  to  perhaps  six  months  after 
birth  about  one-third  of  the  root  will  have  been  formed.  (See  Fig.  98.) 
The  root  end  is  widely  open  (unformed)  and  the  margins  are  thin  and 
sharp.  A  very  vascular  tissue  occupies  the  space  between  the  root 
and  the  bone  and  fills  the  interior  of  the  root.  Meanwhile  the  crown 
cusp  has  advanced  from  the  situation  shown  in  Fig.  96  to  a  point 
just  beneath  the  mucous  membrane,  which  is  pressed  up  and  stretched 
over  the  advancing  tooth  crown,  presenting  to  oral  view  a  tumefied 
condition  more  or  less  corresponding  to  the  form  of  the  crown. 
This  is  nicely  shown  in  Fig.  170,  A  and  B. 

These  anatomical  data  serve  for  the  consideration  of  the  causes 
and  process  of  eruption. 

Causes  of  Eruption.  It  is  evident  that  there  are  forces  which 
can  bring  about  the  elevation  of  a  tooth  crown  from  its  bed  in  the 
crypt  to  its  position  in  the  mouth. 

The  consideration  of  these  has  caused  the  development  of  the 
following  rational  theories,  as  well  as  others  now  obsolete: 

12 


178  DENTITION. 

1.  That  crown  elevation  is  due  to  the  lengthening  of  the  root — 
i.  e.,  as  root  tissue  is  formed  by  the  pulp  and  follicular  wall  lying 
beneath  and  to  the  side  of  its  edges,  the  tooth  is  mechanically  pushed 
up,  more  root  is  formed,  and  a  further  extrusion  occurs.  It  is  to  be 
noted  that  the  root  end  occupies  the  same  level,  at  all  stages  of  eruption, 
in  the  developing  jaw  that  w^as  occupied  by  the  cervical  edge  of  the 
crown  (Fig.  171).  As  no  two  bodies  may  occupy  the  same  space  at  the 
same  time,  the  root-forming  pulp  and  follicular  w^all  push  the  tooth  up  to 
gain  room  for  more  root  formation.  The  pressure  of  the  soft  tissues 
against  the  root  end  is  explained  by  Constant  to  be  derived  from  the 
normal  blood  pressure.^  That  such  an  internal  pressure  exists  is 
shown  by  the  extrusion  of  ordinarily  confined  parts  w'hen  released 

Fig.  170. 


B 

Xiines  of  incision  in  lancing:  A,  A,  over  the  molars;    B,  B,   over  the  cuspids  and  incisors 
before  eruption;   C,  C,  over  the  molars  and  cuspids  after  partial  eruption. 

from  the  accustomed  pressure.  A  simple  accident  demonstrated  this 
to  the  editor.  While  excavating  with  a  large  bur  the  softened 
dentine  about  a  decayed  pulp  chamber,  the  cementum  was  widely 
removed  from  the  pericemental  tissue  beneath  which  latter  fortunately 
remained  unbroken.  It  immediately  protruded  into  the  perforation. 
Constant  also  cites  the  extrusion  of  a  tooth  in  pericementitis  as  an 
evidence  of  the  influence  of  the  blood  pressure.  Another  evidence  is 
the  occasional  rapid  advance  of  a  tooth  after  lancing  of  the  gum. 

2.  The  process  of  tooth  development  is  a  vital  process,  and  that 
of  eruption  has  been  held  also  to  be  (Tomes).  That  cells  concerned 
in  development  seem  to  have  a  predestined  end  or  function  cannot  be 
denied;  at  the  same  time,  throughout  dental  development,  defined 
resistances  to  opposing  forces  seem  to  play  a  part  in  the  moulding  of 

1  International  Dental  Journal,  June,  1903. 


DENTITION. 


179 


the  soft  and  hard  tissues — e.  g.,  the  invagination  of  the  enamel  organ 
by  the  papilla. 

3.  Peirce^  holds  that  the  impact  of  blows  upon  the  jaws  causes  the 
tooth  to  rise  toward  the  gum.  He  explains  the  eruption  of  crowns 
without  roots  upon  this  theory. 

4,  Tomes  explains  the  eruption  of  teeth,  after  development  of  the 
root,  upon  the  theory  that  the  closing  in  of  the  alveolar  process  or 
contraction  of  the  alveolus  upon  the  pericementum  (follicular  wall) 
causes  the  lifting  up  of  the  tooth.  That  such  a  closure  occurs  about 
the  extruding  roots  of  teeth  left  after  the  breaking  away  of  the  crowns 
is  shown  by  examination  of  the  sockets  of  such  roots.  An  abnormally 
shallow  alveolus  closed  by  deposition  of  bone  at  its  apex  will  be  found 


Fig.  171. 


""■nV 


'"    *-  \  aift  '^,  ■"*!!!!  ,.  *.^  ''f  ",  -/  ,  ^-   'H   r 


Diagram  showing  the  upward  movement  of  the  crown  during  eruption  and  root  development. 

(Constant.) 

in  cases  of  small  apical  portions  of  roots  so  extruded.  Upon  the  whole 
Constant's  theory  of  blood  pressure  seems  the  most  satisfactory 
explanation  of  tooth  elevation  under  any  circumstances. 

The  Process  of  Dentition.  At  varying  ages,  according  to  the 
state  of  tooth  development,  the  formed  crown  of  the  tooth  advances 
and  presses  upon  the  follicular  wall  overlying  it  ;  this  is  resorbed, 
the  overlying  tissue  is  reached,  and  osteoclasts  remove  this  as  well 
as  the  upper  edge  of  the  wall  of  the  crypt;  the  mucous  membrane 
is  pushed  up  and  moulded  over  the  crown,  thereby  causing  a  tume- 
faction. 

The  mucous  membrane,  at  first  normal  in  color,  becomes  slightly 
hyperiemic  and  then  changes  to  an  ischsemic  condition  and  whitens 


1  American  System  of  Dentistry. 


180  DPJXTITIOX. 

cwing  to  the  removal  of  the  blood  by  the  pressure  of  the  underlying 
crown.  Resorption  from  beneath  causes  a  break  in  the  continuity  of 
the  mucous  membrane  and  the  crown  tip  erupts  into  the  mouth 
(Fig.  170,  C). 

The  rate  of  resorption  and  crown  advance  are  equalized  in  perfectly 
normal  dentition. 

The  crown  rises  from  the  gum,  is  directed  by  the  tongue  and  lip 
or  cheek,  and  finally  meets  its  antagonists  of  the  opposite  jaw.  The 
interlocking  of  cusps  and  meeting  of  occlusal  surfaces  limit  further 
movement  of  position. 

Meanwhile  root  development  proceeds  and  as  it  occurs  the  alveolar 
process  is  built  about  the  pericementum,  which  has  been  drawn  up 
from  the  follicular  wall.  By  this  means  the  roots  are  firmly  implanted. 
The  further  development  of  the  root  proceeds  until  complete,  and  so 
remains  until  normal  resorption  of  the  temporary  roots  occurs,  and  for 
life  in  the  permanent  teeth. 

The  state  of  formation  of  the  roots  of  temporary  teeth  at  any 
given  age  may  be  judged  by  the  table  of  averages  shown  by  Peirce 
in  Fig.  98.  Being  but  averages,  allowance  for  delays  must  be 
made. 

Apart  from  the  presence  of  the  temporary  teeth  the  process  of 
eruption  is  identical  in  both  sets  of  teeth. 

Periods  of  Eruption.  As  a  general  rule,  the  eruption  of  the 
deciduous  teeth  may  be  said  to  begin  about  the  seventh  month  after 
birth,  and  is  completed  somewhere  about  the  twenty-fifth  month. 
This  rule,  however,  varies  within  wide  limits;  some  children  may  be 
born  with  teeth  erupted;  again,  the  initiation  of  the  process  may  not 
occur  until  the   twelfth  month  or  even  later. 

The  incisor  teeth  are  usually  erupted  in  pairs,  the  molars  and 
cuspids  making  their  appearance  in  fours,  the  first  molars  in  one  group, 
the  cuspids  in  another,  and  the  second  molars  in  a  third  group.  The 
several  groups  require  different  lengths  of  time  to  complete  their  erup- 
tion, the  time  occupied  in  the  eruption  of  the  first  molars  being  longer 
than  that  required  for  the  eruption  of  the  other  groups.  Between  the 
appearance  of  additional  groups  of  the  teeth  an  interval  elapses,  no 
doubt  a  physiological  provision,  for,  as  will  be  shown  later,  the  process 
of  dentition  is  usually  accompanied  by  evidences  of  more  or  less  local 
disturbance,  frequently  by  disturbances  throughout  the  intestinal  tract, 
and  even  reflex  disorders  of  the  central  nervous  system  occur.     It  is 


DENTITION 


181 


believed,  therefore,  that  the  period  which  elapses  between  the  eruption 
of  the  dental  groups  permits  the  organism  to  recover  from  the  effects 
of  previous  disturbance  before  the  new  source  of  irritation  appears. 


Table. 


Group  1. 

Lower  central        i 

Time  of  eruption,  | 

Duration  of  eruption. 

Interval, 

2  to  3  months. 

incisors.                 ' 

7  months.            : 

1  to  10  days. 

Group  2. 

Upper  central  and 

Time  of  eruption, 

Duration  of  eruption, 

Interval, 

2  months. 

lateral  incisors. 

9  months. 

4  to  6  weeks. 

Group  3. 

Lower  lateral 
incisors. 

Time  of  eruption, 
12  months. 

Group  4. 

First  molars. 

Time  of  eruption, 
14  months. 

Duration  of  eruption, 
1  to  2  months. 

Interval, 

4  to  5  months. 

Group  5. 

Cuspids. 

Time  of  eruption, 
18  months. 

Duration  of  eruption, 
2  to  3  months. 

Interval, 

3  to  5  months. 

Group  6. 

Second  molars.      j 

Time  of  eruption, 
26  months. 

Duration  of  eruption, 
3  to  5  months. 

In  the  above  table  it  will  be  noted  that  the  time  of  eruption  of 
the  lower  lateral  incisors  is  later  than  that  of  the  eruption  of  the 
upper  lateral  incisors.  The  reverse  course  is  frequently  observed; 
indeed,  it  has  usually  been  accepted  as  the  rule  of  precedence  in  the 
United  States.  All  tables  as  to  periods  of  eruption  give  but  the 
approximate  times;  while  variations  are  extremely  common.  The  ages 
given  in  this  table  are  those  at  about  which  the  several  teeth  may  be 
expected  to  make  their  appearance.  Stellwagen  (the  American  editor 
of  Coleman),  in  commenting  upon  this  table,  states  that  the  periods  of 
eruption  in  this  country  are  from  one-seventh  or  more  earlier  than  the 
dates  given.  He  suggests  that  the  difference  in  food-habit  may  account 
for  the  differences  in  time. 

Pari  passu  w^th  the  development  and  eruption  of  the  teeth  occur 
developmental  changes  in  all  of  the  glandular  appendages  of  the 
alimentary  canal;  probably  the  alterations  in  their  structure,  and  no 
doubt  in  their  physiological  chemistry,  are  accompanied  by  dental 
provision  for  the  mechanical  subdivision  of  foods  of  postinfantile 
character. 

Symptoms  of  Eruption.  Slight  local  disturbances  are  so  common 
in  even  so-called  normal  first  dentition  as  to  be  accepted  as  physio- 
logical. The  resorption  about  the  tip  of  the  crown  of  the  tooth 
implies  a  condition  of  mild  non-septic  inflammation  at  that  point.  In 
more  marked  cases  there  is  evidence  of  some  irritation  cognizable  to 
the  infant ;  the  gum  is  of  a  somewhat  deeper  color  and  its  temperature 
is  elevated.  Relief  is  afforded  by  pressure,  which  temporarily  reduces 
the  hypersemia,  and  the  child  is  pleased  to  have  its  gums  rubbed,  to 

1  Coleman's  Dental  Surgery.     (SteUwagen.) 


182  DENTITION. 

bite  upon  its  own  or  the  nurse's  fingers,  upon  rings  or  other  objects. 
Still  more  marked  is  the  soothing  effect  of  biting  upon  cokl  substances 
such  as  ice,  which,  in  addition  to  mechanically  lessening  the  blood 
supply,  causes  contraction  of  the  dilated  vessels. 

Slight  reflex  disturbances  are  evidenced  by  the  stimulation  of  the 
salivary  glands,  which  produces  an  increased  flow  of  saliva. 

Reflex  disturbances  of  more  severe  character  occur  in  pathological 
dentition,  to  be  considered  later. 

PATHOLOGICAL  FIRST  DENTITION. 

The  local  disturbances  may  be  exaggerated  beyond  that  degree 
accepted  as  physiological  and  may  be  accompanied  by  nervous,  ali- 
mentary, pulmonary,  or  cutaneous  disturbances.  This  is  pathological 
dentition  and  may  be  of  several  grades  of  severity. 

Causes  and  Pathology.  The  primary  cause  of  pathological  dentition 
may  be  stated  as  an  inequality  in  the  rate  of  gum  resorption  and 
crown  advance.  The  advancing  crown  pressing  upon  the  gum  tissue 
causes  irritation;  the  hypersemia  or  mild  aseptic  inflammation,  instead 
of  remaining  at  a  point  favoring  the  development  of  giant  cells  and 
resorption,  passes  the  physiological  point  and  causes  a  disturbance  of 
function.  Inflammation,  simple  or  even  infective,  may  occur  in  the 
area. 

Swelling  of  the  gum  occurs,  which,  being  distributed  in  all  directions, 
presses  upon  the  crown,  depressing  it  upon  the  pulp  beneath  the 
sharp  root  margins;  at  the  same  time  the  blood  pressure  of  the  pulp 
tends  to  press  the  tooth  upward. 

The  sharp  edges  of  the  root  must  irritate  the  sensitive  and  delicate 
pulp  tissue,  which  becomes  hypersemic  and  swollen  and  still  more 
strongly  urges  the  tooth  upward.  Two  sources  of  disturbance  now 
are  possible:  (1)  the  irritated  gum  tissue  and  (2)  the  irritated  pulp 
tissue.  Through  the  intimate  sympathetic  relations  of  the  fifth  cranial 
nerve,  supplied  to  these  parts,  with  the  seventh,  ninth,  and  tenth 
cranial  nerves  in  the  floor  of  the  fourth  ventricle  of  the  brain,  salivary, 
muscular,  nervous,  alimentary,  and  pulmonary  disturbances  become 
possible. 

Any  systemic  disturbance — e.  g.,  smallpox,  general  debility,  etc. — 
which  lowers  the  nutritive  function  in  the  parts  associated  with  the 
teeth  may  favor  the  production   of  local   pathological  phenomena. 


PATHOLOGICAL  FIRST  DENTITION.  183 

Again,  systemic  disturbance  readily  produces  a  hypersesthesia  of  the 
nervous  system,  favoring  the  production  of  nervous  phenomena. 

Pathological  dentition  may  occur  in  the  absence  of  an  evident 
hypersemic  gum  tissue.  The  tissue  may  be  white,  showing  ischsemia 
from  pressure,  a  binding  down  of  the  root  end  upon  the  pulp  being 
proven  by  the  subsidence  of  symptoms  after  lancing,  and  sometimes 
by  the  rapid,  partial  eruption  of  the  tooth  immediately  after  lancing. 

Again,  pathological  phenomena  have  been  noted  where  no  super- 
ficial local  disturbance  was  evident.  In  these  cases  the  deeper  tissues 
may  exert  a  restraining  influence  upon  the  crown. 

Symptoms.  The  symptoms  of  pathological  dentition  are  both  local 
and  general. 

Local  Symptoms.  The  local  symptoms  are  usually  those  of  inflam- 
mation, red  and  swollen  gum  tissue  at  times  assuming  a  dusky  hue. 
The  gums  may  be  white,  indicating  their  tense  stretching  over  the 
crowns.  Evidence  of  local  irritability  is  given  by  the  fact  that  the 
child  resists  the  touching  of  the  gums,  seizes  the  breast  or  bottle  nipple 
and  immediately  releases  it. 

The  readiness  with  which  the  child  will  take  cold  substances,  ice 
or  ice-water,  is  notable  and  self -explainable.  Alternate  excessive  flow 
of  saliva  and  oral  dryness  is  present.  In  the  gum  over  the  erupting 
tooth  there  may  exist  a  vesicular  enlargement  containing  fluid.^ 

In  the  more  marked  cases  of  local  disturbance  evidences  of  bacterial 
infection  of  the  mucous  membrane  of  the  mouth  may  make  their  ap- 
pearance, such  as  ulcerative  stomatitis.  ^^Tiile,  as  a  rule,  the  breaking 
down  and  ulceration  of  the  tissue  are  confined  to  the  parts  overlying 
the  erupting  teeth,  a  general  stomatitis  or  widely  scattered  patches 
of  ulceration  may  make  their  appearance.  The  localized  condition 
has  been  called  odontitis  infantum. 

General  Symptoms.  The  general  symptoms  may  be  differentiated 
into  mild  and  severe. 

The  mild  symptoms  are  such  as  are  attendant  upon  severe  and 
painful  inflammations  about  the  face  at  almost  any  age ;  thus  anorexia, 
fretfulness,  anger,  restlessness,  sleeplessness,  thirst,  mild  fever,  and 
evident  desire  for  the  upright  position  occur.  The  pain  is  at  times 
paroxysmal,  but  may  become  continuous. 

These  symptoms  subside  upon  the  eruption  of  the  tooth  or  lancing, 
though  erupting  cuspids,  bound  by  a  ring  of  tense  gum  tissue  or  by 

1  Tomes,  System  of  Dental  Surgery. 


184  DENTITION. 

adjoining  teeth,  may  continue  the  irritation  even  when  apparently 
erupted  (Fig.  170,  C). 

The  more  severe  general  symptoms  are  such  as  are  brought  about 
by  reflex  neuroses. 

The  roots  of  the  fifth  cranial  nerves  supplied  to  the  teeth  are  in 
intimate  relation  with  the  roots  of  the  seventh,  ninth,  and  tenth  cranial 
nerves  in  the  floor  of  the  fourth  ventricle,  as  well  as  with  other  cranial 
nerves.  It  may  be  argued  upon  a  'priori  grounds  that  irritation  of  the 
peripheral  ends  of  the  fifth  in  the  pulp  tissue  may  therefore  readily 
produce  neurotic  results  in  the  brain,  salivary  glands,  skin,  lungs  or 
larynx,  intestinal  canal,  or  muscles  of  the  face  or  extremities. 

Taking  the  intestinal  canal  as  the  most  complicated  example,  we 
find  the  following  data:  The  stomach  and  intestines  are  under  the 
influence  of  the  pneumogastric  nerve,  which  sends  to  its  muscular  coats 
both  stimulant  and  inhibitory  fibres.  Likewise,  it  sends  vasomotor 
fibres  to  the  intestines,  division  of  which  leads  to  inhibition  of  the 
muscular  fibres  of  the  vessels  and  leads  to  vasodilatation  and  a  great 
increase  of  very  watery  succus  entericus.^ 

Intestinal  Disturbances.  That  intestinal  disturbances  may  arise 
independently  of  teething  is  self-evident.  They  are  most  liable  to  so 
occur  during  the  very  period  during  which  teething  may  be  supposed 
to  act  as  a  primary  cause  of  intestinal  troubles;  hence  differentiation 
becomes  important. 

That  the  conditions  may  be  associated  is  also  evident.  As  a  rule, 
intestinal  disturbances  arise  from  improper  feeding,  the  food  acting 
as  an  indigestible  irritant  to  the  stomach  and  intestines.  Fermentation 
due  to  bacteria  ensues,  and  diarrhoea  and  colic  are  a  natural  result. 

Musser^  attributes  these  cases  to  development  of  the  bacillus  coli 
communis  and  bacterium  lactis  aeriformis  existing  harmless  in  the 
normal  intestine,  but  developing  under  the  abnormal  conditions. 

This  occurring  in  warm  weather  when  the  child  suffers  from  intense 
heat  has  a  very  debilitating  if  not  fatal  result. 

The  condition  may  be  viewed  as  an  infective  diarrhoea  following  a 
vasomotor  disturbance  of  the  intestinal  walls  set  up  by  reflexes  primarily 
caused  by  the  indigestible  food. 

A  similar  train  of  circumstances  may  be  caused  by  teething. 
Peripheral  irritation  of  terminals  of  the  fifth  nerve  in  the  pulp  may, 
through  the  tenth  nerve,  cause  a  reflex  vasomotor  dilatation  in  the 

1  Halliburton,  Kirke's  Physiology,  1896,  p.  684.  -  Medical  Diagnosis. 


PATHOLOGICAL  FIRST  DENTITION.  185 

walls  of  the  intestines — i.  e.,  hypersemia,  a  condition  which  favors 
bacterial  invasion.  Intestinal  digestion  is  disordered  and  an  infection 
ordinarily  resisted  occurs. 

Diarrhoea  may  follow.  In  either  case  alimentation  is  interfered  with 
and  the  general  nutrition  suffers.  The  child  is  debilitated  by  lack  of 
nutrition;  moreover  toxic  substances  are  generated  in  the  intestine  which 
cause  a  toxeemia,  to  which  many  of  the  general  symptoms  may  be 
attributed.  The  general  debility  also  further  interferes  with  the  pro- 
cess of  dentition. 

Diagnosis.  A  diarrhoea  due  to  improper  feeding  would  not  be 
preceded  by  symptoms  of  pathological  dentition,  would  have  a  history 
of  improper  feeding,  and  possibly  of  unhygienic  conditions,  such  as 
unsterilized  milk  or  milk  bottles,  filthy  surroundings,  etc.  There  is 
a  catarrhal  diarrhoea  accompanied  by  vomiting  and  further  constant 
acid,  watery  stools.  The  stools  may  have  a  chopped-spinach  char- 
acter.    There  is  colic  due  to  collections  of  gas. 

Such  an  infective  diarrhoea  may  readily  follow  the  reflex  and  debil- 
itating effects  of  pathological  dentition,  as  shown  above. 

White'^  has  noted  that  a  choleraic  diarrhoea  may  accompany  and  be 
a  sign  of  pathological  dentition.  Barrett"  states  that  a  diarrhoea  due 
to  dentition  will  probably  be  followed  by  constipation. 

A  symptomatic  diarrhoea  will,  as  a  rule,  be  accompanied  by  signs 
of  pathological  dentition  at  points  in  the  jaws  at  which  teeth  should 
be  in  process  of  eruption. 

Nervous  Disturbances.  Disorders  referable  to  the  central  nervous 
system  are  the  most  alarming  and  are  those  indicating  the  higher 
grades  of  severity  of  irritation. 

The  milder  forms  of  these  are  faint  muscular  twitchings  and  evidences 
of  slight  cerebral  disturbance. 

Either  of  these  may  be  the  result  of  poisons  absorbed  from  the 
alimentary  canal  during  the  course  of  intestinal  fermentation,  but  as 
cases  of  even  convulsions  have  occurred  without  other  cause  than 
teething  apparent  and  been  relieved  by  lancing  alone,  the  possibility 
of  direct  connection  between  teething  and  central  nervous  disturbance 
must  be  admitted'. 

A  distressing  symptom  not  easy  to  elicit  on  account  of  the  age  of 
the  patient  is  headache.  The  child  is  sleepless,  and  cries  without 
apparent  cause;  it  becomes  quiet,  partially  from  exhaustion,  and  after  a 

1  American  System  of  Dentistry.  -  Oral  Pathology  and  Practice. 


186  DENTITION. 

period  again  commences  sobbing.  The  indication  of  central  disturb- 
ance may  at  times  be  noted  in  the  contracted  pupils  of  the  eyes  and 
in  throbbing  arteries.  The  usual  treatment,  the  administration  of 
chloral  hydrate  and  potassium  bromide,  with  cold  a])plications  to  the 
head,  furnishes  relief,  which  is  frequently  not  complete  without  atten- 
tion to  the  dental  organs. 

In  the  more  severe  and  dangerous  cases  the  evidences  of  disorder 
of  the  central  nervous  system  become  unmistakable.  These  appear 
as  clonic  convulsions  or  symptomatic  eclampsia.  While  it  is  probable 
in  many  cases  that  reflex  irritation  from  the  process  of  dentition  in 
itself  is  but  a  secondary  cause  of  convulsions,  yet  evidence  is  sufficient 
to  warrant  its  being  regarded  as  a  determining  factor.  In  very  many 
cases  teething  convulsions  appear  to  indicate  a  neurotic  family  taint, 
and  eclampsia  may  attend  many  disorders  in  children  of  this  type, 
notably  the  mechanical  and  chemical  irritation  induced  by  the  presence 
of  large  masses  of  indigestible  food  in  the  intestines. 

So-called  teething  convulsions  occur  usually  at  a  time  when  several 
teeth  are  in  process  of  eruption.  The  onset  of  the  convulsion  is 
rarely,  although  apparently  often,  sudden.  If  the  child  be  closely 
observed,  it  is  noted  that  a  period  of  cerebral  disturbance — fretful 
crying,  evidences  of  headache,  sleeplessness,  etc. — is  followed  by  a 
period  of  dulness  and  somnolence,  or  the  child  may  lie  with  eyes 
half-open.  Twitching  of  one  or  more  groups  of  muscles  may  be 
observed;  the  orbicularis  oris  and  other  muscles  of  the  lips,  and  the 
muscles  of  the  eye,  notably  the  superior  and  internal  recti,  may  con- 
tract spasmodically.  A  common  muscular  spasm  ushering  in  convul- 
sions is  that  of  the  adductor  muscles  of  the  thumb;  the  thumbs  are 
drawn  toward  the  palms  of  the  hands.  The  adductor  muscles  of 
the  feet  contracting,  the  feet  are  drawn  inward.  This  period  may 
be  ushered  in  by  a  sharp  cry,  the  eyes  roll  upward  with  the  lids 
half-open,  and  consciousness  is  lost.  The  symptoms  may  disappear, 
the  child  awakening  dazed  and  fretful;  or  it  may  sink  into  sleep. 
Unless  the  source  of  irritation  be  removed,  or  active  therapeutic 
measures  be  instituted,  the  eclampsia  may  return  and  in  severe  cases 
be  the  precursor  of  death. 

Infantile  paralysis  of  a  group  of  muscles  or  even  a  single  muscle 
has  been  recorded,  lasting  from  a  few  days  to  months,  appearing  with 
dentition  and  disappearing  after  it.  In  some  cases  it  persists  for 
life.^ 

1  White,  American  System  of  Dentistry. 


PATHOLOGICAL  FIRST  DENTITION.  187 

Skin  Disorders.  It  is  so  common  as  to  be  almost  termed  the  rule 
to  find  that  when  there  are  intestmal  symptoms  there  are  eruptions 
observable  on  the  skin.  The  mildest  form  of  these  is  an  herpetic  erup- 
tion about  the  mouth;  in  other  cases  papular  and  vesicular  eruptions 
are  observed  upon  the  skin  of  the  body  and  limbs. 

Occurring  within  the  mouth  infection  may  be  added  and  ulcerative 
stomatitis  may  occur  upon  the  gums,  tongue,  lips,  or  inside  of  the 
cheek. 

Pulmonary  Symptoms.  Pulmonary  irritation  may  be  expressed  in 
laryngeal  cough  attending  the  eruption  of  teeth  and  disappearing 
thereafter. 

Treatment  of  Pathological  First  Dentition.  This  may  be  divided  into 
prophylactic  and  remedial.  The  prophylactic  measures  include  care 
as  to  Pasteurization  of  milk  or  modified  milk  diet,  sterilization  of 
bottles,  bottle  nipples  and  rings,  the  prevention  of  the  introduction  of 
unclean  fingers  into  the  mouth  of  the  child,  and  the  antiseptic  care 
of  its  mouth  by  frequent  washings  with  a  saturated  solution  of  boric 
acid  in  water.  This  last  may  be  applied  to  the  mouth  on  a  soft  linen 
rag  wrapped  on  the  forefinger.  These  measures,  together  with  the 
proper  feeding,  ventilation,  and  care  as  to  clothing  tend  to  prevent 
intestinal  fermentation  and  to  reduce  the  general  irritability  of  the 
infant. 

Remedial  Measures.  To  reduce  local  hypersemia  of  the  gum 
above  an  erupting  tooth  a  common  domestic  measure  is  valuable,  viz., 
a  small  block  of  ice  is  placed  in  a  clean  napkin,  and  confined  in  place 
by  a  knot;  the  infant  places  it  in  its  mouth  at  pleasure  if  old  enough, 
or  the  nurse  permits  the  child  to  bite  upon  it.  The  mechanical  effect 
of  biting  upon  a  hard  substance  has  added  to  it  a  degree  of  cold  which 
lessens  the  local  vascular  engorgement. 

Any  severe  local  irritation  about  erupting  teeth  should  be  relieved 
by  thorough  lancing  of  the  gum.  It  is  irrational  that  the  child  should 
be  permitted  to  suffer  from  local  irritation  which  may  develop  into 
more  serious  complications. 

This  operation  is  performed  by  dividing  the  gum  lineally  over  the 
incisors  and  cuspids  before  eruption,  crucially  over  the  cuspids  after 
eruption  of  the  cusps  only,  crucially  over  the  upper  first  molar,  and 
with  an  X  incision  over  the  upper  second  and  lower  first  and  second 
molars  (Fig.  170). 

For   severe  cases  Flagg   advised  the   removal  of   a  block  of   gum 


188  DENTITIOX. 

from  over  a  molar.  A  cut  is  made  parallel  with  the  lingual  side 
of  the  crown,  a  second  parallel  with  the  buccal  side,  a  third  parallel 
with  the  mesal  side.  A  tcnacidum  is  thrust  into  the  block  of  gum, 
which  is  drawn  tense  and  then  divided  at  the  distal  portion,  preferably 
with  a  pair  of  curved  gum  scissors.  Lacking  these  latter  the  bistoury 
may  be  used. 

The  cut  over  the  upper  incisors  should,  if  possible,  be  made  a  little 
to  the  outside  of  the  cutting  edge,  that  for  the  lower  to  the  inside, 
in  order  that  their  crowns  may  take  a  proper  direction  toward  occlu- 
sion. 

The  instrument  to  be  used  is  a  sharp-pointed  bistoury,  as  it  pene- 
trates well  and  permits  a  free  draw  cut.  It  is  to  be  wrapped  with 
tape  or  a  strip  of  linen  cloth  until  only  a  half-inch  of  the  point  is 
exposed.  This  precaution  prevents  accidental  wounds.  The  child 
must  be  securely  held  by  an  assistant  the  least  sympathetic  avail- 
able. 

Flagg's  method  was  to  place  the  child  upon  its  back  across  the  lap 
of  the  assistant,  who,  in  one  position,  places  his  left  hand  over  the 
child's  eyes,  securing  the  head ;  his  right  hand  secures  the  hands  upon 
the  abdomen,  while  the  legs  are  held  against  his  body  by  the  right 
arm.  The  position  may  be  exactly  reversed.  The  feet  should  be 
placed  toward  the  light  for  the  upper  jaw,  the  reverse  for  the  lower 
jaw.  In  another  position  the  child  sits  upon  one  thigh  of  the  assistant, 
the  back  of  the  head  resting  upon  the  chest,  and  the  hand  of  that  side 
(usually  the  right)  pressed  upon  the  child's  forehead  to  hold  the  head 
firmly.  The  other  hand  and  forearm  hold  the  child's  arms  and  legs 
firmly. 

The  operator  encloses  the  gum  about  the  part  to  be  cut  with  the 
thumb  and  forefinger  of  the  left  hand,  so  that  the  bistoury  cannot  slip 
and  cut  lip,  cheek,  or  tongue.  Incision  over  the  erupting  tooth 
should  be  made  until  the  knife-blade  is  felt  to  touch  the  enamel 
surface.  The  operation  of  scarifying  the  gums,  making  merely  a  few 
scratches  to  relieve  engorged  vessels,  is  but  temporizing  with  the  con- 
dition; the  cut  should  be  of  sufficient  extent  to  entirely  remove  tension 
from  above  the  tooth.  The  little  finger  of  the  right  hand  may  rest  upon 
the  chin  of  the  child  as  an  additional  guard. 

If  the  child  bite,  a  cork  with  a  string  attached  for  safety  may  be 
used  as  a  prop. 

More  or  less  bleeding  follows  upon  the  operation,  and,  as  a  rule. 


PATHOLOGICAL  FIRST  DENTITION.  Ig9 

ceases  spontaneously.  A  short  period  of  bleeding  is  desirable,  so  that 
vascular  engorgement  may  be  reduced.  Suckling  the  infant  usually 
serves  to  check  the  bleeding;  the  tissues  about  the  cut  surfaces  are 
compressed  by  tongue  and  lips  during  suckling,  and  bleeding  ceases. 
In  the  event  of  the  bleeding  continuing  the  mouth  should  be  carefully 
examined,  and  a  piece  of  ice  in  a  napkin  may  be  given  the  child  to 
suck.  The  child  may  swallow  the  blood  and  later  regurgitate  it. 
Obstinate  bleeding  may  require  the  use  of  styptics,  but  these  should  be 
of  a  character  to  cause  only  coagulation  of  the  blood,  not  the  destruc- 
tion of  tissue.  A  little  powdered  tannin  laid  upon  the  cut  acts  promptlv, 
as  does  also  a  small  amount  of  powdered  alum. 

Death  has  occurred  from  hemorrhage  due  to  lancing  in  cases  of 
presumably  hemorrhagic  diathesis ;  so  that  inquiry  as  to  family  history 
would  be  a  wise  precaution.  Obtaining  such  a  history  the  gravity  of 
the  symptoms  alone  warrant  the  operation.  In  the  absence  of  such 
a  history  the  operation  is  to  be  held  as  trivial.     (See  Haemophilia.) 

The  operation  of  lancing  is  warranted  even  when  the  gum  may 
be  likely  to  heal  over  the  tooth  by  formation  of  cicatricial  tissue, 
provided  symptoms  demand  it. 

Tkeatment  of  Stomatitis.  Should  general  stomatitis,  with  or 
without  stomatitis  ulcerosa,  make  its  appearance,  the  mouth  is  to  be 
promptly  and  freely  sprayed  with  a  3  per  cent,  solution  of  hydrogen 
dioxide,  followed  by  a  spray  of  potassic  chlorate  (gr.  xx-§j),  which 
usually  affords  prompt  relief.  Should  the  spots  of  ulceration  not 
disappear  promptly,  the  mouth  and  tissues  about  the  ulcer  are  to  be 
guarded  by  soft  linen  napkins;  each  ulcer  is  dried  and  touched  with 
carbolic  acid,  full  strength.  The  spraying  is  to  be  repeated  at  intervals 
of  three  hours  during  the  waking  period.  This  method  of  treatment 
is  productive  of  decidedly  better  results  than  follow  the  use  of  the 
common  formula  of  honey  and  borax. 

Teeatmext  of  Skix  Eruptions.  The  eruptions  which  appear 
upon  the  skin  during  dentition  may  be  a  source  of  annoyance  to  the 
child  by  causing  itching.  As  a  rule,  measures  directed  toward  a 
regulation  of  the  intestinal  functions  cause  a  disappearance  of  the 
skin  affections.  If  the  eruption  be  widespread  and  cause  much  itching, 
a  wash  of  phenol-sodic|ue  diluted  to  one-third  with  water  usually 
affords  relief.  If  the  surfaces  be  then  dried  and  talc  powder  dusted 
over  them  the  condition  is  much  alleviated.  About  the  mouth  and 
over  excoriated  surfaces  an  ointment  of  zinc  oxide  is  useful. 


190  DENTITION. 

Treatment  of  Intestinal  SyjMptoms.  The  fermentative  material 
in  the  bowel,  together  with  the  great  mass  of  bacteria  present,  should 
be  removed  by  the  use  of  a  cathartic.  It  is  indicated  in  both  consti- 
pation and  diarrhoea.  Castor  oil  serves  well  and  is  readily  taken  by 
children.  To  lessen  the  irritation  of  the  bowel  laudanum  and  powdered 
acacia  may  be  added. 

The  following  formula  may  safely  be  used  even  at  six  months  of  age : 


^- 

— Tincturse  opii. 

gtt.  X. 

Olei  ricini, 

fSjss. 

Pulveris  acacise, 

5ij. 

Saccharin, 

gr.  ij.. 

Aquae  cinnamomi, 

q.  s.  ad    fsiij. — M. 

Sig. — Shake  the  bottle,  and  give  one  teaspoonful  each  two  hours  if  needed. 

For  an  additional  six  months  of  age  ten  drops  more  of  laudanum 
may  be  added  to  the  general  formula. 

Following  catharsis,  antacid  sedative  astringents  and  intestinal  anti- 
septics are  indicated: 

Jt — Salol,  5j. 

Bismuthi  subnit.,  5ij. 

Misturse  cretae,  ad     fSiij. — M. 

Sig. — One  teaspoonful  every  four  hours.  (Biddle.) 

Or, 

9; — Tincturae  opii,  gtt.  xvj. 

Bismuthi  subnit.,  5ij. 

Misturae  cretae,  3jss. 

SjT.  simp.,  3Jss. — M. 

Sig. — Shake  well,  and  give  in  teaspoonful  doses  every  four  hours.      (Barrett.) 

The  virtues  of  both  formulae  may  be  obtained  by  including  the 
laudanum  (gtt.  xii)  with  the  salol  formula. 

Listerine  in  10-drop  doses,  in  water,  every  three  hours,  serves  as  an 
intestinal  antiseptic. 

The  gums  are,  of  course,  to  be  lanced  at  the  outset  if  the  diarrhoea 
be  due  to  pathological  dentition.  Following  the  intestinal  antisepsis 
the  general  debility  and  possible  intestinal  toxaemia  (see  page  102)  is 
to  have  careful  attention,  and  the  child's  food  is  to  be  properly  adjusted 
to  its  needs.^ 

Treatment  of  Nervous  Conditions.  If  nervous  reflexes,  great 
irritability  or  cerebral  congestion  appear,  attention  shovild  be  directed 
to  the  condition  of  the  bowels  and  the  teeth. 

If  constipation  or  diarrhoea  exist  a  cathartic  is  given  and  the  gums 
lanced.    A  cerebral  sedative  is  to  be  prescribed. 

1  See  works  on  diseases  of  children. 


PATHOLOGICAL  FIRST  DENTITION.  I91 

Jt — Chloral  hydrat.,  gr.  ij. 

Sodii  brom  ,  gr.  v. 

Aquse  raenthse  pip.,  f5ij. — M 

Sig. — Per  orem.     One  dose;  enlarge  formula  for  repetition  as  needed. 

If  convulsions  be  threatened,  the  clothing  should  be  loosened  and 
cool  applications  made  to  the  head. 

If  the  child  be  in  convulsions,  it  should  be  immersed  to  the  waist 
in  water  as  hot  as  can  be  borne,  to  which  has  been  added  two  table- 
spoonfuls  of  common  mustard  flour,  and  cool  water  poured  over  its 
head,  when,  as  a  rule,  the  symptoms  promptly  subside.  Chloroform, 
which  children  endure  well,  may  be  administered. 

After  immersion  a  rectal  injection  of  a  drachm  of  glycerin  or  a 
glycerin  suppository  will  usually  cause  a  free  stool.  A  cerebral 
sedative  should  be  administered. 

J^ — Chloral  hydrat.,  gr.  ij. 

Sodii  brom.,  gr.  v. 

Starch  paste,  Sij. — M. 

Sig. — To  be  administered  per  rectum.  (Atkinson.) 

It  is  well  also  to  administer  a  cathartic  to  unload  the  intestines  of 
irritating  substances  possibly  present. 

After  sleep,  if  appearances  indicating  dental  irritation  be  observed, 
gum  lancing  is  practised.  It  is  wise  that  this  operation  be  thus  deferred, 
as  convulsions  may  be  precipitated  by  the  act  of  lancing  when  the 
nervous  system  of  the  child  is  overexcited.  The  removal  of  intestinal 
irritants  by  a  cathartic  given  per.  orem  is  also  in  order  before  lancing. 

It  has  been  repeatedly  noted  that  where  evidence  of  marked  cerebro- 
spinal irritation  is  present,  for  which  no  probable  source  can  be  assigned 
and  an  examination  of  the  gums  shows  no  apparent  local  disturbance, 
yet  if  it  be  at  a  period  when  one  or  more  teeth  are  in  process  of  eruption, 
but  are  still  covered  or  bound  down  by  gum  tissue,  if  gum  lancing 
be  practised  relief  is  immediate  and  the  lancing  may  even  avert  a 
threatened  attack  of  eclampsia.  It  is  presumed  that  these  are  cases 
of  pulp  irritation  in  which  a  failure  of  resorption  of  tissue  in  advance 
of  the  tooth  crown  has  caused  pressure  upon  the  pulp  forming  the 
root  end. 

Constitutional  States  Modifying  Dentition. 

Children  who  are  the  victims  of  hereditary  syphilis  usually  cut  their 
teeth  very  early,  the  alveolar  process  being  in  many  cases  insufficient. 
Cases  are  recorded  where  children  have  been  born  with  crowns  of  teeth 
visible  upon  the  gum,  there  being  no  evidence  of  root  formation,  the 
crowns  being  loosely  held  to  the  gum  by  fibrous  tissue.    It  is  necessary 


192  DENTITION. 

to  remove  these  loose  crowns  to  permit  the  infant  to  suckle.  Children 
affected  with  rachitis  have  the  process  of  eruption  much  delayed.  It  is 
seen,  therefore,  that  the  presence  of  loose  crowns  of  teeth  is  a  condition 
pointing  to,  though  by  no  means  diagnostic  of,  hereditary  syphilis. 
Long-delayed  eruption  of  teeth  should  prompt  a  search  for  further 
indications  of  rachitis.  Particularly  in  children  in  whom  a  history 
of  hereditary  syphilis  is  obtainable  the  process  of  dentition  may  be 
accompanied  by  rapid  and  frequently  widespread  breaking  down  of 
the  soft  tissues  over  and  about  erupting  teeth.  Local  measures  of 
treatment  seem  to  be  of  but  little  avail,  except  that  antiseptic  treat- 
ment undoubtedly  prevents  complications  from  extraneous  infection. 

In  children  classified  indefinitely  as  strumous,  which  may  mean  the 
children  of  syphilitic  or  tuberculous  parents,  or  those  with  no  such 
history  whose  surroundings  are  of  the  most  unhygienic  kind,  the 
process  of  dentition  may  not  only  have  an  untoward  course,  but 
phagedenic  ulcerations  may  occur.  It  is  usually  in  the  degree  of  a 
child's  debility,  either  inherited  or  acquired  through  improper  care, 
that  dentition  assumes  morbid  features.  The  treatment  of  such  cases 
must  be  directed  to  raising  the  health  standard.  As  local  therapeusis, 
no  measures  seem  more  effective  than  the  sprays  of  hydrogen  dioxide 
first;  next,  potassium  chlorate,  and,  if  conditions  indicate  it,  sprays  of 
dilute  listerine,  which  is  stimulant,  antiseptic,  and  slightly  astringent. 

Infantile  Scurvy.  Cases  are  recorded  in  which  the  improper 
feeding  of  children  has  been  followed  by  evidences  of  scorbutus.  It 
occurs  usually  in  bottle-fed  babies  confined  to  patent  foods.  The 
gums  become  tumid,  and  hemorrhagic  extravasations  occur  in  their 
substance;  the  periosteum  is  stripped  from  the  margins  of  the  alveolar 
walls,  the  soft  tissues  hanging  in  discolored,  pendulous  masses  about 
and  beyond  the  teeth  if  any  be  erupted. 

The  child  is  peevish,  listless,  and  feeble.  There  is  apparent  pain 
in  the  limbs. ^ 

The  treatment  is  largely  systemic  and  consists  of  using  fresh  cows' 
milk  modified  to  conform  to  human  milk,  and  in  the  administration 
of  fresh  lemon-juice,  preferably  boiled,  allowed  to  settle,  and  the 
supernatant  fluid  used.^ 

The  mouth  should  be  sprayed  with  antiseptics, 

'  Hare.  "  Ibid. 


THE  SECOND  DENTITION.  1 93 

THE  SECOND  DENTITION. 

By  reference  to  Fig.  110  it  will  be  seen  that  at  six  and  one-half  years 
of  age  the  twenty  temporary  teeth  are  still  all  in  position,  and  that 
taking  their  places  in  the  line  of  the  arch  are  the  four  permanent  first 
molars,  the  roots  of  which  are  still  incomplete. 

These  molars  do  not  replace  any  temporary  teeth,  but  during  the 
"change"  support  the  jaws  with  the  assistance  of  the  temporary 
molars  until  the  permanent  incisors  are  fully  erupted,  and  with  the  aid 
of  the  incisors  until  the  bicuspids  come  into  occlusion.  Their  office 
as  jaw  props  and  organs  of  mastication  during  the  change  is,  there- 
fore, very  important.  Of  their  later  function  more  will  be  said 
farther  on. 

At  six  and  one-half  years  the  crowns  of  the  permanent  incisors 
lie  in  the  relations  shown  with  the  temporary  central  roots  resorbed 
and  the  lateral  root  partly  so.  Their  crowns  are  practically  complete, 
but  the  roots  are  unformed. 

The  cuspid  crown  lies  well  above  the  unresorbed  temporary  cuspid 
root,  between  the  canine  fossa  and  ala  nasi.  The  roots  of  the  first 
and  second  temporary  molars  a  trifle  resorbed  upon  the  inner  side 
embrace  the  formed  crowns  of  the  first  and  second  bicuspids. 

In  their  crypts  back  of  the  first  molars  lie  the  forming  crowns  of 
the  second  permanent  molars.  The  third  molars  are  not  in  evidence 
in  the  illustration,  but  their  development  is  in  progress. 

It  will  be  seen  that  the  permanent  central  and  lateral  incisors 
replace  the  temporary  central  and  lateral  incisors,  the  permanent 
cuspid  the  temporary  cuspid,  and  the  first  and  second  bicuspids  the 
first  and  second  temporary  molars,  respectively. 

From  this  age  to  adult  age  as  previously  the  jaw  undergoes  constant 
change,  enlarges  by  constant  resorptions  and  depositions  of  bone,  and 
changes  its  contour  to  conform  to  the  changes  occurring  throughout 
the  body,  and  to  accommodate  the  permanent  teeth,  which  are  in  gen- 
eral terms  larger  and  more  numerous  than  the  temporary  teeth. 

It  may  be  said  that  the  alveolar  process  built  about  the  roots  of 
temporary  teeth  and  the  roots  of  the  temporary  teeth  are  all  resorbed 
during  the  replacement  of  the  latter,  and  that  when  the  crowns  of 
the  permanent  teeth  are  fully  erupted  new  alveolar  process  is  built 
up  about  their  roots.  Any  subsequent  change  in  the  position  of  the 
permanent  teeth  is  accompanied  by  an  alteration  in  the  alveolar 
process,  and  after  extraction  the  latter  is  resorbed,  but  upon  an  implan- 

13 


194 


DENTITION. 


tation  (which  see)  being  done  new  process  will  form.    Its  dependence 
upon  the  teeth  is,  therefore,  evident. 

The  following  table  gives  the  approximate  ages  for  the  eruption 
of  the  permanent  teeth: 

First  molars 5%-  7  years. 

Central  incisors 7  -  8  " 

Lateral  incisors 8  -  9  " 

First  bicuspids 10  -11  " 

Second  bicuspids 11  -12  " 

Cuspids 12  -14  " 

Second  molars 12  -15  " 


Third  molars 


.   16    -20      " 
and  indefinitely  beyond. 


The  Process  of  Resorption  of  the  Temporary  Roots.  After  com- 
pletion of  formation  the  roots  of  the  temporary  teeth  remain  in  this 
state  but  a  short  time,  as  their  successors  are  ready  to  advance  to 
their  places. 


Fig.  172. 


n.  I J  -M  wf  .iMj 


Decalcification  of  the  deciduous  teeth.     The  numbers  indicate  years.    Compare  with  Fig.  98.    j 

(Peirce.) 

Comparing  the  ages  at  which  resorption  begins  with  the  ages  at 
which  it  is  complete  (see  Fig.  172),  it  will  be  noted  that  approximately 
three  and  a  half  years  are  required  in  all  cases  for  the  removal  of 
the  temporary  roots. 

xA.t  the  time  the  permanent  tooth  begins  its  advance  it  lies  in  a 
bony  crypt  above  and  lingual  to  its  predecessor,  except  in  the  case 
of  the  bicuspids,  which  lie  between  the  roots  of  the  temporary  molars 
(Figs.  110  and  173). 

Each  crypt  has  its  own  follicular  wall  enclosing  a  permanent  tooth 
crown. 

In  the  follicular  wall  overlying  the  crown  appear  large  multinu- 
cleated cells  the  origin  of  which  is  unknown,  but  which  by  some  are 
thought  to  be  transformed  osteoblasts,  by  others  leukocytes  (Figs. 
173  and  174).  The  latter  is  the  probable  explanation,  as  analogous  cells 
are  found  about  tissues  or  foreign  bodies  about  to  undergo  resorf.tion 


THE  SECOND  DENTITION. 


195 


Fig.  173. 


anywhere  in  the  body.  (See  Resorption.)  In  the  particular  situation 
under  consideration  they  are  called  odontoclasts.  The  tissue  between 
the  root  and  crown  has  by  Tomes  been 
given  the  name  of  the  "  resorbent  organ" 
(Figs.  173,  A,  and  174).  These  giant  cells 
have  a  solvent  or  digestive  function  not 
understood,  but  which  is  competent  to 
remove  both  the  organic  and  inorganic 
matter  of  cementum  and  dentine,  and  evi- 
dences of  action  upon  enamel  in  other 
situations  are  not  wanting.  (See  Resorp- 
tion of  Enamel.)  That  the  solvent  is  acid 
is  shown  by  the  evidence  of  decalcification 
about  the  area  of  resorbed  enamel  of  un- 
erupted  crowns  of  some  permanent  teeth. 
It  is  a  curious  fact  that  no  evidence 
of  decalcification  of  the  permanent 
crown  has  been  demonstrated  to  result 
from  the  proximity  of  the  multinucleated 
cells  in  cases  of  physiological  resorption       ot.     •     .i.     w 

1-      -J  c>  r  Showing  the  relations  of  an  erupt- 

of     temporary     roots.        In     all     probability     ing  permanent  tooth  to  its  deciduous 
,,  ,    .  1       J     1    1         ,1  predecessor:  A,  A,  A,  odontoclasts. 

the  enamel  is  protected   by  the    presence 

of  Nasmyth's  membrane,  which  is  resistant  to  acids.    These  cells  are 

probably  invited  by  irritation  due^^to  pressure  of  the  advancing  per- 


FiG.  175. 


The  structure  of  the  resorbent  organ,  show- 
ing multinucleated  or  giant'cells  (odontoclasts). 
(Tomes.) 


i  i^ 


Imprisonment  of  second  temporary 
molar;  resorption  of  its  roots,  with  ab- 
sence of  second  bicuspid.  (Skiagraph 
by  Custer.) 


manent  tooth  crown,  as  the  resorption  is  almost  always  found  at 
the  point  of  approximation  of  the  crown  with  the  root,  or,  in  other 
words,  at  the  pressure  point  (Fig.  176). 

Cases  of  resorption  of  temporary  roots  without  the  presence  of  a 


196 


DEXTITION. 


permanent    crown    are,  however,  noted    and    exjilained    by  Tomes 
upon  the  ground  that  resorption  is  a  vital  act  independent  of  the  press- 


Fin.  176. 


Fig.   177. 


Phases  of  resorption  of  temporary  roots.     (Skiagraphs  by  Price.') 

ure  exerted  (Fig.  175).  As  resorption  of  permanent  roots,  however,  has 
often  occurred  from  pressure  of  the  crown  of  another  tooth  and  occurs 
at  the  pressure  point  in  physiological  resorption,  local- 
ized irritation,  even  in  the  absence  of  a  permanent 
crown,  must  be  credited  with  a  large  influence  in  the 
process.  It  is  to  be  remembered  also  that  in  the  ab- 
sence of  the  pressure  resorption  often  does  not  occur 
— e.  g.,  when  laterals  are  absent  and  the  permanent 
cuspids  erupt  to  the  side  of  the  deciduous  cuspids 
(Fig.  179). 

According  to  Tomes  redeposition  of  cementum  oc- 
curs in  previously  resorbed  areas  upon  temporary  roots, 
a  fact  corresponding  with  effects  noted  in  permanent 
roots.     (See  resorption  of.) 

As  the  root  of  the  temporary  tooth  disappears  the 
pulp  continuously  fuses  with  the  resorbent  organ,  so 
that  when  the  crown  alone  remains  the  pulp  is  still 
vital  (Fig.  173).  At  times  it  seems  to  take  up  the 
resorbent  function  and  resorbs  the  crown  dentine  in 
some  cases  almost  entirely.  In  one  specimen  a  circum- 
scribed portion  of  the  cementum  and  of  enamel  were 


Diagram  illus- 
trating the  rela- 
tion of  a  resorbed 
temporary  root 
and  the  perma- 
nent tooth,  also 
the  involvement 
of  the  pulp  as  a 
part  of  the  re- 
sorbent organ. 
Resorption  of  the 
interior  of  crown 
of  a  temporary 
tooth. 


1  Items  of  Interest,  1901. 


THE  SECOND  DENTITION. 


197 


removed  by  it  at  the  point  of  junction.  This  constituted  practically  a 
case  of  perforation  by  resorption  (Fig.  177).  At  times  bay-like  exca- 
vations in  the  crown  dentine  occur.  When  the  root  resorption  reaches 
the  point  shown  in  the  central  incisor  in  Fig.  1 10  the  temporary  tooth  is 
loosened,  moves  about,  and  annoys  the  child,  who  may  pick  it  out,  or 
it  is  removed  by  extraction. 

Formation  of  the  Roots  of  Permanent  Teeth.  The  extent  of  root 
development  at  any  age  is  of  great  importance  in  view  of  canal  thera- 
peutics. Unformed  roots  present  a  mechanical  difficulty  of  sealing 
the  apex  of  the  canal.  The  size  of  the  pulp  at  the  apical  foramen 
of  such  teeth  contraindicates  the  use  of  arsenic  and  even  pressure 
anaesthesia  is  often  unsuccessfully  applied. 

Fig.  178. 


Absence  of  upper  left  lateral  incisor,  with  permanent  cuspid  in  its  place;  two  temporary 
cuspids  retained.     Man,  aged  twenty-five  years. 

The  roots  are  developed  in  precisely  the  same  manner  as  in  the 
case  of  the  temporary  teeth,  by  the  combined  deposition  from  the 
follicle  wall,  which  is  drawn  up  on  the  root  as  a  pericementum  and 
from  the  papilla,  which  is  drawn  up  as  a  pulp  (Fig.  100). 

The  extent  of  development  of  any  of  the  permanent  teeth  may  be 
seen  at  a  glance  by  reference  to  the  valuable  table  of  Peirce  (Fig.  107). 
So  graphically  does  this  table  give  the  desired  information  that  expla- 
nation becomes  unnecessary. 

Irregularities  of  Second  Dentition.  Some  temporary  teeth  may 
be  retained  long  after  adult  age  is  reached.  The  teeth  most  subject 
to  this  are  the  cuspids  and  second  temporary  molars. 


198 


DENTITION. 


In  the  case  of  the  cuspids,  the  permanent  cuspid  is  delayed  or 
takes  an  unusual  direction,  erupting  lingually  or  labially,  or  at  times 
being  directed  into  the  place  normally  occupied  by  the  lateral  incisors, 
which  are  wanting,  or  very  rarely  the  cuspid  erupts  posteriorly  to  the 
first  bicuspid.  At  about  forty  years  of  age  the  temporary  cuspids  may 
be  lost  by  resorption  of  their  roots,  but  until  such  time  should  be 
retained  if  usefully  filling  a  space.  If  in  interference  with  proper 
alignment  or  eruption  of  the  permanent  cuspid  they  should  be  ex- 
tracted. Their  late  resorption  is  somewhat  pathological  in  character 
and  probably  due  to  or  incited  by  a  partial  resorption  of  the  root  end 
during  the  descent  of  the  permanent  cuspid. 

Fig.  179. 


Absence  of  upper  lateral  incisors  and  right  bicuspid. 

From  an  adult. 


Retention  of  temporary  cuspids. 


The  late  enforced  loss  of  the  temporary  cuspid  indicates  the  advis- 
ability of  an  implantation  operation  (Fig.   179). 

The  molars  are  retained  as  a  rule  because  of  an  absence  of  perma- 
nent crowns  to  cause  resorption,  although  this  may  occur  without 
such  pressure  (Fig.  175).  I  have  seen  a  case  of  an  adult  lady  with 
eight  deciduous  molars  in  place.  The  question  of  the  abnormal 
development  or  absence  of  permanent  germs,  or  of  the  state  of 
the  roots  of  the  temporary  tooth  may  be  settled  by  the  x-vajs  (Figs. 
175  and  176). 

The  question  of  extraction  or  retention  depends  upon  the  diagnosis. 
When  retention  of  temporary  molars  and  cuspids  occurs,  they  are 


PATHOLOGICAL  SECOND  DENTITION.  199 

apt  to  occupy  an  occlusal  level  lower  than  that  of  the  permanent 
teeth  (Fig.  175).  They  may  not  be  in  occlusion  at  all,  as  was  the 
case  with  the  eight  molars  just  referred  to.  This  proves  the  fact 
that  the  general  occlusal  level  of  the  permanent  teeth  is  farther  from 
the  margin  of  the  alveolar  process  than  in  the  case  of  the  temporary 
teeth.    The  length  of  the  permanent  crowns  accounts  for  this. 

The  maxillary  and  alveolar  development  which  occurs  during  the 
years  occupied  by  the  "change"  due  to  second  dentition  and  the 
eruption  of  the  second  and  third  molars  must  also  be  borne  in  mind. 
The  form  of  the  lower  jaw  at  the  angle  changes.  The  ramus  becomes 
pronounced  and  the  jaw  lengthens  from  the  ramus  to  the  symphysis. 
Corresponding  changes  occur  in  the  upper  jaw.  The  antrum  enlarges 
and  the  tuberosity  becomes  pronounced  in  correspondence  with  the 
development  of  the  upper  maxilla  and  the  eruption  of  the  teeth,  in 
the  consideration  of  which  both  predestination  to  a  typical  form  and 
dynamic  influences  are  to  have  weight. 

Disorders  of  the  Second  Dentition.  The  devitahzation  of  the  pulp 
of  a  temporary  tooth  and  proper  canal  filling  delays  but  does  not 
absolutely  prevent  resorption.  Chronic  abscesses  upon  such  roots 
destroy  the  resorbent  organ,  but  some  pathological  resorption  may 
occur,  as  in  case  of  permanent  roots  (which  see).  Pus  has  an  alkaline 
reaction  which  may  neutralize  the  acid  solvent.  As  a  rule  such  roots 
are  mechanical  obstructions  to  the  permanent  crowns,  which  are 
deflected  to  one  side  and  caused  to  erupt  irregularly;  again,  the  tempo- 
rary root  may  be  bodily  pushed  aside,  its  apex  pressed  against  the 
alveolar  process  and  gum  tissue,  which  are  resorbed  and  the  necrotic 
root  end  is  seen  extruded  labially  through  the  gum.  Extraction  is  indi- 
cated. 

When  temporary  roots  are  not  thus  mechanically  removed  they  are 
gradually  extruded  and  decayed,  or  suppurative  processes  cause  the 
resorption  of  the  process  about  them. 

Injudicious  retention  of  temporary  teeth  may  thus  cause  an  irregu- 
larity. On  the  other  hand,  premature  extraction  by  permitting  the 
approximation  of  the  previously  erupted  permanent  teeth  may  have 
an  equally  bad  effect  upon  an  erupting  tooth  (Fig.  183). 

In  anticipation  of  physiological  resorption  of  temporary  roots,  all 
temporary  teeth  should  be  carefully  watched,  cleansed,  filled,  and,  if 
necessary,  their  roots  treated  so  that  a  normal  replacement  by  the 
permanent  teeth  may  occur.  If  pronounced  disease  occurs  just  pre- 
vious to  the  time  for  normal  replacement,  extraction  is  indicated. 


200  DENTITION. 

It  will  be  recalled  that  the  teeth  are  an  evolution  of  the  dermoid 

system,  which  fact  possesses  pathological  significance  in  certain  acute 

and  specific  skin  diseases.     It  is  noted  in  some  cases  of  the  eruptive 

fevers  of  children,  particularly  when  the  child  is  much  debilitated,  that 

after  the  cessation  of  the  acute  disease  a  necrotic 

Fig.  180.  «.       • 

,  .,.  ,j.  affection  of  the  jaw  occurs,  involving  the  alveolar 

bone  and  its  contents.  As  many  of  these  cases 
occur  between  the  ages  of  three  and  seven  years, 
the  temporary  teeth  are  still  in  situ ;  these,  with 
the  partially  developed  permanent  teeth  and  the 
enclosing  bone,  may  be  exfoliated.  The  necrotic 
process  may  involve  but  one  tooth,  or  may  include 
Effects  of  the^ema-  ^^^  ^^  *^^  temporary  teeth,  their  successors,  and  a 
ture  loss  of  a  deciduous     large  mass  of  bouc.^     The  disease  w4th  which 

second  molar.  ,  .  .      .  „  ,  .  ,   . 

this  necrosis  is  most  frequently  associated  is  scar- 
let fever  ;^  it  is  also  found  as  a  sequel  of  measles  and  smallpox.  It 
will  be  observed  that  all  of  these  diseases  are  forms  of  specific  der- 
matitis, and  the  teeth  as  part  of  the  dermoid  system  are  affected.  (See 
Chapter  IX.)  "The  cases  prior  to  exfoliation  of  the  bone  exhibit  a 
stripping  of  the  periosteum,  apparently  beginning  about  the  necks  of 
the  teeth.  A  discharge  of  pus  having  a  fetid  odor  is  present,  and  the 
soft  tissues  may  be  raised  from  the  bone  for  a  variable  extent;"  that  is, 
there  is  evidence  of  purulent  periostitis.  In  the  course  of  some  weeks, 
six  or  eight,  the  necrotic  bone  and  its  contents  exfoliate.  Salter  ob- 
serves that  the  sequestra  forming  after  severe  scarlet  fever  are  much 
more  extensive  than  those  which  form  as  a  sequel  of  measles. 

The  administration  of  mercurials  has  been  credited  with  such  a 
loss  of  teeth  and  process.  I  have  been  shown  a  sequestrum 
containing  three  teeth  attributed  to  this  cause.  In  these  cases  the 
parts  should  be  kept  as  aseptic  as  possible  by  means  of  hydrogen 
dioxide  and  the  compound  tincture  of  capsicum  and  myrrh  (enough 
to  cloud  a  glass  of  water)  used  as  a  stimulant  mouth  wash.^  When 
loose  the  sequestrum  should  be  removed.  The  parts  heal  by  gran- 
ulation if  due  attention  be  paid  to  the  general  physical  welfare  of 
the  child. 

Eruption  of  the  Molars.  The  first  permanent  molars  rarely  produce 
more  than  slight  rheumatic  pains.  The  gum  irritation  may  be  relieved 
by  an  X  incision,  or  at  times  by  the  application  of  phenol-sodique 

1  Salter,  Dental  Pathologj-.  ^  Ibid. 

^  Garretson,  A  System  of  Oral  Surgery.  • 


PATHOLOGICAL  SECOND  DENTITION.  201 

and  laudanum,  equal  parts,  with  the  finger-tip.  A  little  alcohol  or 
dilute  tincture  of  iodine  serves  almost  equally  well. 

As  some  time  may  elapse  between  eruption  and  occlusion  the  first 
molars  do  not  receive  a  proper  friction.  Associated  frequently  with 
carious  temporary  teeth,  they  are  frequently  decayed  in  their  sulci  and 
fissures;  to  prevent  this  it  has  been  recommended  that  oxyphosphate 
of  zinc  be  placed  over  these  fissures  without  previous  excavation.^ 

The  lower  second  molars  may  cause  some  irritation  owing  to  an 
insufficient  development  of  the  jaw  at  the  angle,  leaving  an  inadequate 
accommodation  for  the  crown.  At  about  nine  years  of  age  the  second 
molar  occupies  the  angle  of  the  jaw  in  much  the  same  position  as 
shown  in  Fig.  101  for  the  third  molar.  If  held  back  a  pathological 
condition  equivalent  to  that  occurring  in  the  temporary  teeth  may 
result;  reflexes  producing  heavy  pains  about  the  jaw  or  worse  effects, 
such  as  epileptiform  convulsions,  may  be  produced. 

Truman^  has  prevented  a  threatened  second  attack  of  this  sort  by 
deep  incisions  in  the  gum  over  the  site  of  the  crown.  The  presump- 
tion is  that  such  treatment  relieves  the  tension  upon  the  pulp  under- 
lying the  developing  root. 

The  third  molars  frequently  induce  pathological  conditions. 

The  upper  third  molar  meeting  in  its  descent  the  roots  of  the  second 
molar  may  be  united  to  it  by  hypercementosis — the  condition  of  con- 
crescence (which  see) ;  escaping  this  it  may  meet  a  dense  palato-alveolar 
plate  of  bone  at  the  tuberosity  and  be  deflected  buccally  through 
the  thinner  buccal  plate  of  bone,  so  that  its  occlusal  face  presents 
cheekward  (Fig.  181).  Here  retained  food  collects  about  it  and  caries 
occurs,  or  a  suppurative  inflammation  of  the  cheek  or  free  gum  margin 
may  occur.  For  this  condition  sterilization,  free  incision  of  the  gum 
margin,  and  subsequent  asepsis  maintained  by  antiseptic  sprays  will 
reduce  the  inflammation,  which,  however,  is  apt  to  recur  at  intervals. 
If  the  cheek  be  irritated  or  the  position  of  the  tooth  permanently 
fixed,  only  traction  of  the  tooth  into  a  correct  position,  grinding  away 
of  the  sharp  cusps,  or  extraction  will  alleviate  the  condition.  The 
extraction  of  such  a  tooth  is  little  loss  to  the  individual.  The  possi- 
bility of  concrescence  in  such  a  case  as  shown  in  Fig.  181  must  be 
considered  when  extraction  is  intended.  Individual  motion  is  diag- 
nostic. 

The  pressure  of  an  erupting  third  molar  upon  the  second  molar 
may  cause  neuralgic  pains,  and  at  times  the  teeth  in  general,  as  far 

1  L.  Ashly  Faught.  ^  International  Dental  Journal,  1899. 


202 


DENTITION. 


forward  as  the  central  incisor,  may  seem  to  loosen  up  and  become 
tender  to  touch  and  again  become  comfortable  and  tight.  These 
symptoms  may  be  repeated  apparently  in  consonance  with  the  efforts 
at  eruption. 

Owing  to  insufficient  development  at  the  angle  of  the  jaw  it  is 
almost  the  rule  that  the  eruption  of  the  third  molar  is  attended  with 
some  degree  of  discomfort  due  to  gum  and  bone  irritation  and  possibly 
to  pressure  on  the  formative  pulp  (Fig.  182). 

For  some  months  prior  to  eruption  heavy,  gnawing,  rheumatic  pains 
may  be  indefinitely  located  about  the  jaw  and  ear  of  the  affected  side. 
The  muscles  of  mastication  become  stiff  and  may  contract  spasmodic- 
ally, simulating  trismus.  These  symptoms,  if  severe,  may  be  relieved 
by  deep  X  incisions  in  the  gum;  or,  if  mild,  by  the  application  of  non- 


FiG.  181. 


Fig.  182. 


Abnormal  eruption  of    the  upper  third 
molar. 


Partial  eruption  and  impaction  of  third 
molar.    (Skiagraph  by  Custer.) 


discoloring  rubefacients  or  sedatives  to  the  outside  of  the  face,  over 
the  affected  parts.  The  massage  of  the  parts  affords  some  relief. 
Flagg^  recommended  the  following: 

]^ — Tinct.  opii, 
Tinct.  aconiti, 

Chloroformi,  da     q.  s. — M. 

Sig. — To  be  rubbed  on  the  outside  of  the  face. 

Or, 

T^ — Aconitine,  gr.  j. 

Cerat.  simp.,  5j. — M. 

Sig. — To  be  well  spatulated.     To  be  distended  with  oil  of   cloves  or    campho-phenique 
and  gently  rubbed  on  the  outside  of  the  face,  the  mouth  and  eyes  to  be  particularly  avoided. 

Or,  when  the  aconitine  fails  to  produce  relief: 

Jfc — Veratrine,  gr.  xx. 

Cerat.  simp.,  .)j. — M. 

Sig. — To  be  used  in  the  same  manner  as  the  aconitine. 

As  the  tooth  advances  the  symptoms  may  become  progressively 
severe.     The  gum  may  become  inflamed,  swollen,  and  be  masticated 


'  Dental  Cosmos. 


PATHOLOGICAL  SECOND  DENTITION.  203 

upoiij  the  oral  pyogenic  organisms  produce  infection,  presumably  find- 
ing an  entrance  at  the  point  proximating  the  second  molar.  The 
patient  suffers  from  the  pain  and  inability  to  masticate  and  becomes 
nervous,  irritable,  and  debilitated;  the  breath  becomes  fetid  and  the 
salivation  excessive.  The  inflammation  extends  into  the  contiguous 
tissues,  and  pus  may  form,  extending  into  them;  all  mastication  is 
prevented,  fever  is  present,  and  the  patient  prostrated;  septicgemia 
and  death  may  follow.^ 

Results  similar  to  these  may  occur  when  the  crown  is  partly  erupted, 
being  covered  at  its  distal  portion  by  a  curtain  of  gum  which  may  be 
ulcerated  upon  its  under  surface. 

In  these  latter  cases  the  pus  as  a  rule  finds  egress,  but  occasionally 
it  burrows  into  the  pocket  between  the  tooth  and  contiguous  tissue, 
causing  much  inflammation. 

Treatment.  The  treatment  depends  upon  the  stage  to  which  the 
inflammation  has  advanced. 

If  the  patient  be  able  to  partly  open  the  mouth  the  part  may  be 
sterilized  by  spraying  it  with  a  germicide  such  as  a  1  :  2000  solution 
of  mercuric  chloride  in  hydrogen  dioxide.  Following  this  an  injection 
of  cocaine  solution  is  made  into  the  gum  tissue  or  flap  of  tissue  and 
the  gum  completely  removed  from  over  the  face  of  the  crown. 

To  accomplish  this  a  deep  linear  cut  is  made  with  a  sharp  bistoury,  ex- 
tending from  the  distolingual  to  the  mesolingual  angle  of  the  crown. 
A  similar  cut  is  made  from  the  distobuccal  to  the  mesobuccal  angle. 
If  not  already  free  the  gum  is  divided  at  its  mesal  contact  with  the 
distal  surface  of  the  second  molar.  The  block  is  now  penetrated  by 
a  tenaculum,  drawn  tense,  and  the  final  cut  made  at  the  distal  border 
with  decidedly  curved  gum  scissors. 

The  hydrogen  dioxide  spray  should  be  again  applied  to  remove  any 
possible  pus  germs  present  and  should  be  repeated  at  intervals  of 
about  two  hours.  A  neglect  of  this  simple  precaution  cost  the  editor 
a  week's  personal  discomfort  and  ability  to  masticate  after  the  removal 
of  a  trifling  and  apparently  non-inflamed  flap  of  gum.  A  cold  compress 
should  be  recommended  for  the  angle  of  the  jaw  if  deemed  advisable. 
Magnesium  sulphate  as  a  derivative  may  be  used  with  advantage. 

If  the  patient  be  confined  to  his  bed  and  unable  to  open  the  jaws 
a  more  difficult  operation  presents.  The  first  object  should  be  to 
reduce  the  intensity  of  the  inflammatory  symptoms.  This  is  accom- 
plished by  the  removal  of  the  gum  block  as  above  if  the  mouth  can 

1   Flagg,  and  occasional  reports. 


204  DENTITIOX 

be  opened  sufficiently.  Etherization  may  be  resorted  to,  after  oral 
sterilization,  for  the  purpose.  A  jaw  separator  is  introduced  and 
operated  until  sufficient  space  is  gained  and  the  cuts  made.  If  no 
more  be  possible  at  the  first  visit  the  lingual  and  buccal  linear  cuts 
should  be  made  to  ensure  free  blood-letting,  which  may  be  increased 
by  syringing  forcibly  with  luke-warm  water,  the  position  of  the  patient 
being  such  that  gravity  favors  its  flowing  out  of  the  mouth. 

Cold  compresses  are  to  be  placed  over  the  angle  of  the  jaw  and 
magnesium  sulphate  and  the  hot  pediluvium  administered  as  deriva- 
tives.   The  antiseptic  sprays  are  to  be  used  as  before  directed. 

If  in  addition  local  massage  over  the  angle  of  the  jaw  be  practised 
the  swelling  and  muscular  hardness  usually  disappear  in  a  few  days. 

It  is  well  to  then  remove  the  entire  block  of  gum  to  prevent  re- 
infection. 

If  the  third  molar  be  correctly  placed  its  eruption  as  a  rule  proceeds 
uninterruptedly  from  this  point,  though  it  may  never  be  entirely  free 
from  some  degree  of  overlapping  by  the  gum  tissue.  Pockets  are 
thus  formed  w^hich  favor  food  retention,  which,  undergoing  fermenta- 
tion, may  either  cause  ulceration  of  the  soft  parts  or  caries  of  the 
distal  and  distobuccal  surfaces  of  the  tooth. 

More  marked  malposition  may  cause  difficulty  of  eruption,  necessi- 
tating the  extraction  of  the  third  molar  or  even  of  the  second  molar. 

In  some  cases  it  may  be  better  to  extract  the  upper  third  molar,  as 
it  will  probably  elongate  in  time. 

A  presentation  of  the  occlusal  face  of  the  third  molar  to  the  distal 
surface  of  the  second  molar  is  the  most  common  form  of  malposition. 

If  very  deep  seated  the  third  molar  may  at  times  be  diagnosed  in 
this  position  by  passing  an  explorer  or  thin  right-angled  blade  down 
the  distal  surface  of  the  second  molar,  or  by  means  of  a  deep  incision 
with  a  bistoury.  Failing  this  or  preferably  replacing  it,  the  a*-rays 
are  a  very  valuable  means  of  diagnosis. 

In  this  situation  pathological  resorption  of  the  root  of  the  second 
molar  may  result  and  irritation  of  its  pulp  be  added  as  a  complication. 
In  this  case  the  second  molar  must  be  extracted. 

A  more  common  form  of  presentation  exhibits  the  distal  surface  of 
the  crown  above  the  gum  and  the  mesoocclusal  angle  locked  beneath 
the  cervix  of  the  second  molar  (Fig.  182).  The  third  molar  may  be  re- 
moved by  an  operation  involving  the  surgical  removal  of  a  portion  of 
the  base  of  the  coronoid  process  followed  by  extraction.  The  pulp  of 
the  third  molar  may  be  devitalized  by  arsenic  applied  and  sealed  in 


PATHOLOGICAL  SECOND  DENTITION.  205 

a  pit  drilled  in  its  distal  surface.  After  death  of  a  portion  of  the  pulp 
the  pit  may  be  made  to  perforr.te  the  crown  from  side  to  side,  and 
then  a  dentate  fissure  bur  mounted  in  the  right-angle  handpiece  may 
be  used  to  saw  off  the  occlusal  half  of  the  crown.  In  the  space  thus 
gained  and  between  the  second  and  third  molars  a  wedge  of  seat-angle 
may  be  neatly  fitted;  its  swelling  causes  mutual  separation,  which 
loosens  the  third  molar  somewhat  by  the  process  of  resorption.  It 
should  now  be  quite  readily  extracted  by  appropriate  movements. 

Cryer  recommends  the  removal  of  the  occlusal  section  of  the  crown 
of  the  third  molar  by  means  of  a  carborundum  disk,  and  the  removal 
of  the  tooth  by  means  of  forceps  or  elevators. 

The  loss  of  a  second  molar  may  be  for  other  reasons  necessary, 
but  such  a  loss  in  the  last  case  described  is  equivalent  to  a  loss  of 
two  teeth,  as  the  third  molar  will  be  of  little  value. 


CHAPTER    IX. 
MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Abnormalities  of  the  teeth  are  found  associated  with  position/size^ 
form,  and  structure.  Aberrations  in  form,  structure,  and  size  are 
included  under  the  head  of  malformations  of  the  teeth ;  aberrations  of 
position  are  discussed  under  the  head  of  malpositions  of  the  teeth. 
The  particular  section  of  dentistry  relating  to  malpositions  of  the 
teeth  is  by  general  consent  made  a  special  department  of  operative 
dentistry,  that  of  orthodontia;  but  many  of  the  phases  of  the  subject 
are  of  great  pathological  interest,  although  the  therapeutic  measures 
usually  demanded  are  mechanical  in  character  and  clearly  belong  to 
the  fields  of  operative  and  prosthetic  dentistry. 

Malformations  of  the  teeth  may  be  macroscopic  or  visible  to  the 
naked  eye,  or  microscopic,  requiring  special  preparation  for  observation 
under  the  microscope. 

The  causes  of  imperfectly  formed  enamel  or  teeth  must  be  sought 
by  study  of  the  conditions  preceding  their  development.  That  modi- 
fications of  general  nutrition  must  modify  tooth  development  seems 
to  be  a  safe  proposition. 

An  ill-nourished  child  is  apt  to  have  at  least  poorly  organized  tooth 
material,  while  in  one  that  has  actually  undergone  an  exanthematous 
disease  the  tooth  form  subsequently  seen  seems  frequently  to  have 
been  profoundly  modified  by  the  disease. 

MICROSCOPIC  MALFORMATIONS. 

Microscopic  or  histological  defects  of  the  teeth  may  affect  any  of  the 
dental  tissues,  enamel,  dentine,  cementum,  pulp,  or  pericementum. 

Enamel.  Defects  in  enamel  structure  range  from  any  degree  of 
orderliness  in  the  even  distribution  of  globular  bodies  and  cementing 
substance  in  the  tissue  to  gross  aberrations  in  formation.  The  finer 
variations  of  structure  are  not  easily  recognizable. 

Theoretically  perfect  enamel  should  show  in  longitudinal  section  a 
series  of  squares  of  uniform  size  built  into  rods,  the  spaces  between  the 
squares  and  rods  being  marked  by  lines  of  cementing  substance  having 


MICROSCOPIC  MALFORMATIONS. 


207 


a  refractive  index  slightly  different  from  that  of  the  squares.  While 
such  a  structure  is  perhaps  never  found,  it  is  difficult  to  draw  a  line 
where  aberrations  from  such  a  standard  become  pathological.  An 
arbitrary  standard  might  be  assumed  as  follows:  regard  any  enamel 
as  pathological  where  areas  of  it  differ  from  its  general  substance  to 
such  an  extent  as  to  have  a  decidedly  different  refractive  index,  A 
typical  form  of  abnormality  is  noted  in  what  are  known  as  white  spots 

Fig.  183. 


Portion  of  a  white  spot  in  enamel,  showing  lack  of  interprismatic  cement  substance.     X  2000. 

(Williams.) 


of  the  enamel,  areas  in  which  an  opaque  surface  exists  instead  of  the 
normally  translucent  enamel. 

Opaque  Spots  in  Enamel.  White,  brown,  and  corn-colored  opaque 
areas  of  enamel  are  frequently  seen  surrounded  by  apparently  normal 
enamel. 

^  Examined  without  the  aid  of  the  microscope  they  are  seen  to  present 
a  surface  as  smooth  as  any  enamel,  but  upon  this  surface  being  broken 
up  with  a  bur  a  chalky,  granular,  whitish  material  containing  at  times 


208     MALFORMATIOXS  AXD  MALPOSITIOXS  OF  THE   TEETH. 

the  yellowish  pigment  is  seen  sometimes  occupying  the  entire  thickness 
of  the  enamel. 

Williams  submitted  the  enamel  at  the  borders  of  such  spots  to 
microscopic  examination  and  compared  it  with  enamel  in  the  first 
stages  of  decay,  finding  in  both  a  similar  appearance  characteristic 
of  a  lack  of  or  a  loss  of  interprismatic  cement  substance  (Fig.  183; 
also  Fig.  301). 

Fig.  1S4. 


Section  through  humau  cuspid,  showing  sulcus  and  apijearance  of  tissue  in  its  vicinity. 
X  75.     (Specimen  by  Choquet,  photo,  by  Williams.) 


Upon  the  data  derived  from  his  investigations  with  the  development 
of  the  enamel  he  concluded  that  these  spots  are  due  to  a  lack  of  such 
cement  substance.  This  leaves  as  the  probable  substance  in  the  spot 
unfused  globules  mingled  with  some  pigment. 

Enamel  formation  about  the  sulci  of  teeth  is  frequently  faulty; 
owing  to  an  imperfect  union  of  the  enamel  segments  forming  the  cusps 
of  the  teeth  minute  fissures  exist  in  the  enamel;  these  are  most  marked 
in  the  fissures  of  molars,  as  shown  in  Fig.  184.  The  enamel  bounding 
these  fissures  has  an  irregular  structure. 

The  dentinal  fibrillse  may  penetrate  the  substance  of  the  enamel 
(Fig.  185),  occupying  defined  channels  in  its  substance;  this  is  re- 
garded by  Williams  as  a  developmental  accident.    He  points  out  that 


MICROSCOPIC  MALFORMATIONS. 


209 


the  organic  filaments  from  the  dentine  become  atrophied  with  the 
progress  of  enamel  formation  and  canals  remain.  Caush^  claims 
to  have  found  this  to  be  a  normal  condition  of  human  enamel,  and 
regards  these  as  nutrient  spaces.  (See  p.  141.)  This  condition,  as 
also  many  other  variations  of  structure  found  in  the  dental  tissues 


Ftg.    185t 


"^^^^^i 


w:j\ 


'r^k 


Section  of  human  molar,  showing  dentinal  fibrillae  penetrating  enamel.      X  600.      (Williams.) 

of  man,  are  shown  by  Williams  to  have  their  normal  prototypes  in 
the  dental  tissues  of  lower  animals;  for  example,  the  penetration  of 
dentinal  fibrillae  into  enamel  is  a  normal  condition  in  the  teeth  of  the 
kangaroo.  Such  conditions  are  not  to  be  confounded  with  fissures 
of  enamel  where  large  lines  of  faulty  calcification  or  non-calcification 
extend  through  the  thickness  of  enamel.    K  portion  of  the  enamel,  as 


1  International  Dental  Journal,  June,  1904. 
14 


210     MALFORMATIOXS  AND  MALPOSITIONS  OF  THE  TEETH. 


shown    by  Fig.    186,  may    occupy  an    area    normally  occupied    by 
dentine. 

Enamel,  even  normal  enamel,  is  not  of  uniform  composition;  were 
it  so,  it  would  exhibit,  in  addition  to  an  orderly  arrangement  of  its 
histological  elements,  a  uniformity  in  color.  So  common  are  differences 
in  this  direction  that  the  presence  of  pigment  bands  must  be  regarded 
as  normal.  It  is  the  rule  to  find  enamel  traversed  by  deeply  pigmented 
parallel  bands  (Fig.  115)  which  pass  obliquely  upward  from  the 
surface  of  the  dentine  to  the  surface  of  the  enamel.  These  are  termed 
the  bands  of  Retzius  (see  Chapter  VI.);  they  appear  to  mark  the  size 
of  the  enamel  cap  at  successive  periods  of  its  growth. 

Fig.  186. 


Section  of  human  bicuspid,  showing  mass  of  very  imperfectly  calcified  enamel  projected  into 
the  dentine,  with  coarse  fissures  leading  to  the  surface.     X  75.     (Williams.) 

Stratification  and  striation  of  the  enamel,  as  shown  by  Williams, 
must  be  regarded  as  normal  physiological  records  of  the  mode  of 
enamel  formation.  Kirk  has  shown  that  normal  enamel  shows  vari- 
ations in  density  in  the  same  teeth.     (See  p.  160.) 

All  of  these  histological  defects  represent  variations  of  deposition, 
no  doubt  due  to  fluctuations  of  the  nutritive  processes  of  the  child 
at  the  time  of  tooth  formation.  Histological  records  made  in  the 
enamel  are  not  like  those  made  in  other  tissues,  for  there  is  no  certain 
provision  through  which  such  defects  can  be  remedied  at  subsequent 
periods. 


MICROSCOPIC  MALFORMATIONS. 

Fig.  187. 


211 


Section  of  human  incisor,  showing  "bands  of  Retzius"  and  marked  stratification  of 
enamel.     X  125.     (Williams.) 


Fk;.  1s> 


Section  of  enamel  from  syphilitic  tooth,  with  appearances  ressmbling  the  lacunae  of  cementum. 

X  600.  i (Williams.) 


212    MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Profound  nutritive  disturbances,  such  as  those  attenchng  hereditary 
syphihs  in  children,  affect  the  structures  of  the  teeth.  One  of  the  gross 
resuks  of  this  disease  is  a  common  malformation  of  the  general  form  of 
the  incisors.  The  hard  tissues  of  such  teeth  exhibit  microscopic  evi- 
dences of  faulty  histology;  they  are  dull  and  opaque  and  traversed  by 
irregular  bands.  Viewed  in  section  the  enamel  of  such  teeth  is  seen  to 
be  almost  structureless  (Fig.  188).  Williams  found  that  the  contents 
of  the  large,  irregular  spaces  in  this  enamel  did  not  respond  to  stains — 
i.  e.,  did  not  contain  organic  matter. 

There  is  evidence  that  other  forms  of  specific  dermatitis — scarlet 
fever  and  measles — which  occur  at  an  early  age  may  affect  the  for- 
mation of  enamel.  The  defects  attributed  to  the  exanthemata  are 
irregular  pits  upon  the  crowns  of,  particularly,  the  incisors  (Fig.  189), 
though  the  cuspids  and  first  molars  also  suffer.  In  some  cases  the 
crowns  appear  honey-combed.  The  condition  is  known  as  hypoplasia 
of  the  enamel  and  is  evidently  due  to  an  effect  upon  the  enamel  organs. 

Fig.  189.  Fig.  190. 


Hypoplasia  due  to  eruptive  fevers. 

With  a  history  of  a  case,  including  the  age  of  the  child  at  the  period 
of  the  disease,  if  examination  be  made  of  the  positions  of  the  defects, 
the  age  will  serve  as  an  indication  as  to  whether  there  has  been  any 
connection  between  the  eruptive  fever  and  the  dental  malformation. 
For  example,  if  enamel  pits  upon  incisors  have  been  caused  by  an 
eruptive  fever  between  the  ages  of  four  and  five,  they  should  occupy 
about  the  half-way  area  of  the  crown-face;  it  is  evident  that  the  enamel 
being  already  formed  about  the  cutting  edge  of  the  tooth,  alterations 
of  nutrition  could  not  affect  the  already  formed  tissue.  In  cases 
where  a  causal  association  of  enamel  defects  with  the  eruptive  fever 
is  made  out  with  reasonable  clearness,  it  is  usual  to  find  all  of  the 
crowns  of  the  teeth  which  are  in  process  of  formation  affected  in  a 
similar  manner. 

Cases  are  observed  where  there  has  been  a  formative  crisis  to  the 
extent  of  having  no  enamel  whatever  formed  over  the  occlusal  section 
of  the  crown,  its  deposit  on  the  remainder  of  the  crown  being  quite 
normal  (Fig.  190). 


MICROSCOPIC  MALFORMATIONS.  213 

D.  B.  Freeman^  records  the  case  of  an  individual,  aged  twenty-six 
years,  whose  teeth  anterior  to  the  second  molar  were  entirely  devoid 
of  enamel.  The  condition  was  hereditary;  it  appeared  in  both  brothers 
and  sisters,  and  could  be  traced  back  for  three  generations. 

Hopewell-Smitlr  claims  that  teeth  apparently  devoid  of  enamel 
have,  in  all  cases  examined  by  him,  had  attenuated  enamel  upon 
them.    This  would  also  be  classified  as  hypoplasia. 

Black^  has  described  the  teeth  of  a  man,  aged  twenty-seven  years, 
as  having  enamel  of  an  opaque,  paper-white  appearance,  as  readily 
cut  as  a  slate-pencil,  and  with  dentine  of  ordinary  consistence.  The 
teeth  presented  little  caries.  He  also  described  the  temporary  teeth 
of  a  child  as  all  without  trace  of  enamel,  the  dentine  soft,  bendable 
in  any  direction,  with  production  of  pain,  and  penetrable  with  a  sharp 
explorer  (agenesia  of  enamel). 

Hopewell-Smith*  describes  the  enamel  developed  during  rickets  as. 
faulty,  and,  in  so  far  as  limited  observation  could  determine,  contained 
numerous  spaces  probably  filled  with  soft  tissue.  These  spaces  were- 
in  the  first-formed  portions  of  the  specimens  observed. 

Dentine.  Data  regarding  the  finer. phases  of  defective  histological 
structure  of  the  dentine  are  meagre.  It  has  been  observed  that  the 
dentinal  tubuli  of  some  teeth  are  much  larger  than  in  others  of  the 
same  age,  and,  no  doubt,  future  investigations  with  an  improved 
technique  directed  toward  a  study  of  the  exact  mode  of  dentine 
formation  will  exhibit  defects  more  certainly. 

The  chief  histological  defects  noted  in  dentine  are  areas  of  faulty 
or  non-calcification,  called  interglobular  spaces.  (See  Chapter  VI.) 
These  are  most  common  in  the  dentine  immediately  underlying  its 
covering  tissue,  so  common  in  the  dentine  under  the  cementum  that 
this  portion  of  dentine  has  been  called  the  stratum  granulosum,  the 
granular  layer  of  Tomes  (Fig.  191).  In  the  body  of  the  dentine  these 
spaces  have  a  more  irregular  distribution  (Fig.  118). 

In  wet  ground  sections  (Rose)  the  dentinal  filaments  are  seen  to 
pursue  an  unbroken  course  through  these  areas.  The  contents  of  the 
interglobular  spaces  react  to  stains  like  the  sheaths  of  Neumann;  that 
is,  they  probably  contain  transitional  tissue.  These  areas  probably 
represent,  as  do  defective  spots  of  enamel,  periods  of  depressed  vitality, 
or  of  altered  nutrition.  In  the  light  of  present  knowledge  regarding 
the  subject  they  are  to  be  viewed  as  areas  in  which  the  calcific  process 

1  See  Guilford,  American  System  of  Dentistry,  vol.  iii. 

2  Histology  and  Pathol.  Histology  of  the  Teeth. 

^  Dental  Cosmos,  June,  1898.  *  Loc.  cit. 


214     MALFORMATIOXS  AND  MALPOSITIONS  OF  THE  TEETH. 


Fig.  191. 


was  faulty.    The  malformations  noted  in  connection  with  the  enamel 
of  syphilitic  teeth  have  their  analogues  in  the  dentine  (Fig.  192). 

Interglobular   spaces   afford   some   evidence   of   the   formation    of 
dentine  by  a  deposition  of  globular  bodies  in  a  matrix  of  protoplasmic 

material.  The  continuation  of  the 
tubules  through  the  mass  of  un- 
calcified  contents  is  evidence  of 
their  independent  formation  by  the 
fibril  cells. 

Histological  malformations  of  the 
pulp  have  not  been  recorded,  the 
normal  histology  of  the  organ  not 
beinff  made  out  with  sufficient  cer- 
tainty  to  determine  what  appear- 
ances are  to  be  regarded  as  abnormal.  Grosser  aberrations,  such  as 
those  shown  in  Fig.  151,  are  made  out. 


■^  C    -^  ^' 


Dentinal  tubuli  terminating  in  the  spaces  of 
the  granular  layer.      (Tomes.) 


Fig.  192. 


Section  showing  interglobular  spaces  in  dentine  of  a  syphilitic  human  tooth.      (Williams.) 


Cementum.  x\s  stated  in  Chapter  VI.,  the  pericementum  contains 
numbers  of  multinucleated  cells — odontoclasts;  and  their  presence  is 
not  to  be  regarded  as  abnormal.  The  cementum  of  the  roots  of  teeth 
may  exhibit  evidences  of  former  action  of  these  cells  in  excavations  of 


MACROSCOPIC  MALFORMATIONS. 


215 


cementum  which  by  a  subsequent  deposition  of  cementum  have 
become  filled.  This  gives  an  irregular  course  to  the  cement  laminae 
(Fig.  191).  These  appearances  are  to  be  regarded  as  not  necessarily 
pathological,  for  the  following  reason:  for  some  time  (years)  subse- 
quent to  the  eruption  of  the  teeth  developmental  changes  occur  in 
the  alveolar  bones ;  depositions  (subperiosteal)  increasing  their  volume 
are  accompanied  by  resorption  of  other  portions  of  the  bone,  such  a 
balance  being  kept  between  their  processes  that  the  teeth,  although 
shifting  their  positions,  are  kept  in  normal  occlusion. 


Fig.  193. 


^\\^\\k^M.i\\^\^* 


Section  of  a  bicuspid  with  its  alveolus,  showing  a  pit-like  absorption  upon  the  side  of  the 
root  in  which  the  redeposit  of  the  cementum  has  begun:  a,  dentine;  h,  cementum;  c,  peri- 
dental membrane;  d,  bone  forming  the  wall  of  the  alveolus;  e,  absorbed  area  of  cementum. 
It  will  be  noticed  that  a  new  deposit  of  cementum  has  begun  the  filling  of  the  area,  and  that 
the  soft  tissue  in  the  area  of  absorption  is  of  a  cellular  type.  The  bone  also  shows  the  effects 
of  absorption  in  the  cutting  away  of  portions  of  the  rings  of  the  Haversian  systems  at  /,  while 
at  g  the  presence  of  osteoclasts  shows  that  absorption  is  in  progress  at  that  point.     (Black.) 

The  cementum  may  be  thickened  by  additional  deposits  as  in 
hypercementosis,  which  is  an  excess  of  development  classed  as  patho- 
logical. 

A  small  excrescence  may  be  found  upon  the  cementum,  and  is 
known  as  a  cemental  nodule. 


MACROSCOPIC  MALFORMATIONS. 


The  teeth  may  vary  from  the  normal  either  as  regards  size  or  external 
configuration. 

Variations  as  to  Size.  It  is  patent  to  the  most  casual  observer 
that  the  teeth  vary  as  to  size.  Comparisons  in  this  direction  are  made 
by  an  examination  of  the  upper  central  incisors.    Fig.  194  shows  nearly 


216     MALFORMATIOXS  AND  MALPOSITIOXS  OF  THE  TEETH. 

the  extremes  of  observable  sizes;  Guilford'  points  out  that  excessively 
large  central  incisor  crowns  are  usually  supported  by  abnormally  small 
conical  roots.  INIarked  giantism  of  the  central  incisors  usually  occurs 
in  pairs,  the  other  teeth  being  of  normal  size.  On  the  other  hand, 
dental  giantism  of  less  degree  may  involve  all  of  the  teeth  of  a  denture. 
The  molar  teeth  are  occasionally  of  enormous  size,  the  bicuspids  rarely 
so,  and  the  cuspids  next  in  frequency  to  the  molars  as  to  the  occur- 
rence of  giantism.  Guilford  observes  that  giantism  of  the  cuspid 
crowns,  unlike  that  of  the  central  incisors,  is  usually  accompanied  by 
a  corresponding  size  of  root.  He  mentions  the  case  of  a  cuspid  measur- 
ing an  inch  and  a  half  in  length  from  tip  to  tip. 

Dwarf  Teeth.  Deficiency  in  size  is  of  more  common  occurrence 
than  excessive  size.  It  appears  to  occur  more  frequently  with  the 
upper  third  molars  and  upper  lateral  incisors  than  with  any  other 
teeth.     Fig.   19.5  shows  the  extremes  in  size  between  two  perfectly 

Fig.  194.  Fig.  19.5. 


formed  lower  third  molars.  The  stunting  of  these  and  of  other  teeth 
is,  however,  usually  associated  with  such  an  aberration  of  outward 
form  that  most  dw^arf  teeth  must  be  considered  as  abnormal  in  form 
as  well  as  in  size. 

Conical  Teeth.  The  primitive  tooth  is  composed  of  but  a  single  cone. 
Human  teeth  have  forms  which  are  modified  cones  or  combinations 
of  cones.  Return  to  a  conical  form  is  therefore  denominated  reversion 
to  a  primitive  t}'pe. 

A  central  incisor,  or  more  frequently  a  lateral  incisor,  may  have 
a  conical  crown,  as  shown  in  Fig.  196.    The  condition  may  be  double. 

Upper  third  molars  frequently  consist  of  but  a  single  cone,  diminutive 
in  size;  at  times  a  crater-like  crown  is  formed  by  a  series  of  small  cones 
about  a  central  pit. 

Pitted  and  Grooved  Teeth.  Nutritional  disturbances,  the  exanthem- 
ata, and  s}^hilis  all  seem  to  have  a  profound  influence  upon  the 
form  of  teeth  developing  during  the  period  of  active  disease.     With 

1  American  System  of  Dentistry,  vol.  ui. 


MA  CROSCOPIC  MA  LFORMA  TIONS. 


217 


the  passing  of  this  period  the  development  of  the  tooth  may  proceed 
in  an  orderly  manner. 

The  malformations  described  under  this  heading  may  consist  of  a 
series  of  irregular  grooves  or  pittings,  the  crowns  having  the  general 
normal  outlines 

Of  these  malformations  Figs.  197  and  202  are  fairly  typical. 

Hutchinson  Teeth.  During  the  first  few  weeks  after  birth  skin 
eruptions  characteristic  of  hereditary  syphilis  are  apt  to  occur  in  the 


Fig.  196. 


Tusk-like  permanent  central  incisors,  temporary  teeth  retained  on  either  side. 
Lady,  aged  twenty-five  years. 

contaminated  child.  At  this  period  the  enamel  of  the  tips  of  the 
permanent  incisors  is  undergoing  development  (see  Fig.  107)  and  the 
effect  of  the  eruption  is  to  cause  a  defective  development  at  this  point. 
Instead  of  the  normal  angles  and  flattened  curves  of  the  labial  surfaces 
the  incisors  may  have  a  roughly  rounded  and  stunted  appearance. 
The  incisal  edge  of  the  tooth  is  narrower  than  its  neck.    The  enamel 

Fig.  197. 


Showing  the  front  teeth  grooved  from  the  alternation  of  perfectly   and  imperfectly  developed 
portions  of  enamel.      (Tomes.) 

at  this  edge  is  irregularly  and  badly  formed;  but  there  is  a  semblance 
of  the  three  enamel  tubercles  found  normally.  The  middle  tubercle 
being  composed  of  defective  enamel  is  soon  lost  by  abrasion,  causing 
the  tooth  to  have  a  notched  appearance  (Figs.  199,  200,  201). 

A  lack  of  development  of  the  anterior  portion  of  the  upper  jaw  has 
been  noted  in  a  number  of  cases  clearly  syphilitic  (Fig.  199).    It  has 


218     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

been  noted  that  not  all  syphilitic  children  present  these  dental  appear- 
ances; and  again  appearances  said  to  be  identical  with  them  are 
observed  in  children  said  not  to  be  syphilitic;  nevertheless  the  presence 

Fir,.  198. 


Malformations  of  inci.sal  half  of  crowns,  with  cervical  half  perfect.     Attributable  to 
malnutritional  processes  rather  than  syphilis.     (Model  by  W.  A.  Capon.) 


Fig.  199. 


Hutchinson's  teeth.     Two  upper  centrals  notched  and  contracted.     Characteristically 
undeveloped  upper  jaw.     From  an  hereditary  syphilitic,  aged  twelve  years. 


Fig.  200. 


Fig.  201. 


Syphilitic  teeth  in  upper  and  lower  jaws  as 
they  appear  when  recently  erupted. 


The  teeth  of  hereditary  syphilis 
at  maturity. 


MACROSCOPIC  MALFORMATIONS.  219 

of  such  teeth  is  usually  regarded  as  a  valuable  diagnostic  sign  of 
hereditary  syphilis.  The  existence  of  interstitial  keratitis  and  of 
chronic  catarrh  of  the  middle  ear  in  connection  with  Hutchinson's 
teeth  are  held  to  be  diagnostic  signs  of  hereditary  syphilis  (Hare). 

Therapeutics  based  upon  such  a  diagnosis  are  followed  by  better 
results  as  a  rule  than  when  the  general  indication  is  ignored.  The 
boy  from  whose  mouth  a  model  (Fig.  199)  was  obtained  had  interstitial 
keratitis  in  the  left  eye,  chronic  nasal  catarrh,  and  a  somewhat  flat 
development  of  the  nasal  bones. 

Tomes  favors  and  adduces  evidence  to  support  the  contention  of 
Hutchinson  that  honey-combed  incisal  edges  of  incisors  and  cuspids 

Fig.  202. 


Pitted  and  fringed  teeth,  some  of  them  carious  at  the  incisal  edges.     Specimen  in  museum 
of  Philadelphia  Dental  College. 

and  occlusal  surfaces  of  first  molars  are  indicative  of  mercurials  ad- 
ministered in  early  childhood. 

Pitted,  grooved,  or  otherwise  malformed  teeth  may  decay  sometimes 
so  badly  as  to  produce  a  black,  slimy  appearance  almost  loathsome 
to  view.     In  other  cases  surprisingly  little  caries  develops. 

Treatment.  If  slightly  pitted,  gold  or  porcelain  fillings  may  be 
introduced.  In  some  cases  grinding  off  the  rough  incisal  edge  is 
sufficient;  in  other  cases  the  teeth  may  require  to  be  drawn  down 
after  this  procedure,  or  porcelain  inlays  may  be  used  to  restore  the 
incisal  edges.  In  the  extremely  disagreeable  cases  above  mentioned 
some  form  of  crowning  must  be  resorted  to.  Fig.  203  exhibits  a 
restoration  of  the  case  shown  in  Fig.  198. 


220     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Fusion  of  Teeth.  Two  or  more  teeth  may  be  united  during  the 
process  of  development.  The  union  may  occur  (1)  by  the  crowns, 
(2)  by  the  roots  alone,  and  (3)  by  both  crowns  and  roots. 

Fused  teeth  united  by  the  crowns  alone  have  not  been  shown.  The 
nearest  approach  to  it  is  the  case  illustrated  by  Tomes,  in  which  two 
central  incisors  have  fused  by  union  of  the  crown  portions  and  one- 


FiG.  203. 


Same  as  Fig.  198,  with  Land  jacket  crowns  placed  over  anterior  teeth.     (W.  A.  Capon.) 

fifth  of  the  root  portions  of  the  two  teeth  (Fig.  204).  Such  teeth 
would  have  dentine  common  to  both  crowns  at  the  point  of  union, 
the  enamel  being  reflected  over  the  outside  of  the  common  dentinal 
mass  according  to  the  scheme  shown  in  the  diagram  Fig.  208,  B.  The 
pulp  may  be  common  to  the  two  teeth  in  the  crown.  Of  course,  the 
root  pulps  are  separate. 

Fig.  204. 


Lingual  view.  Labial  view. 

Fusion  of  two  permanent  upper  central  incisors  by  their  crowns  and  a  portion  of  the  roots. 

(Tomes.) 

The  condition  is  a  record  of  the  fact  that  prior  to  dentinification  the 
papillffi  and  enamel  organs  of  the  two  teeth  have  coalesced  at  some 
point.  This  must  have  occurred  at  an  early  period,  perhaps  even  during 
the  descent  of  the  buds  into  the  jaw.  When  it  is  considered  that  the 
two  central  incisors  are  contained  in  two  separate  intermaxillary  bones, 
the  rarity  of  such  a  union  and  in  such  a  manner  may  be  appreciated. 
I  have  seen  such  a  union  between  a  right  lower  central  and  lateral 


MACROSCOPIC  MALFORMATIONS.  221 

incisor  in  the  mouth.     Recession  of  the  gum  permitted  a  view  of  the 
cervical  conformation. 

Those  teeth  united  by  fusion  of  the  roots  have  a  common  dentine 
at  the  point  of  union,  with  cementum  reflected  over  that.  The  pulp 
is  common  to  the  two  teeth  at  the  point  of  fusion. 

Fig.  205. 


T 


a,  fusion  of  two  molars  at  the  roots — two  pulp  ca^dties,  one  foramen;  6,  c,  fusion  of  super- 
numerary teeth  roots  to  buccal  roots  of  upper  molars,  pulp  canal  common  where  probes 
cross;  d,  view  of  resorbed.  root  end  of  two  fused  temporary  teeth;  e,  concrescence  by  hyper- 
cementosis. 

In  the  specimen  shown  in  Fig.  205  at  a  there  is  but  one  apical  fora- 
men. In  that  shown  at  h  and  c  there  is  but  one  foramen  for  the  two 
fused  portions  of  pulp,  though  the  other  canals  have  their  usual  for- 
amina. These  cases  evidence  an  accidental  coalescence  of  pulps  after 
much  independent  root  formation.    Fusion  throughout  both  crowns  and 

Fig.  206.  Fig.  207. 


Fusion  of  temporary  teeth  by  their  Fusion  of  a  supernumerary  tooth  with 

roots.  an  upper  third  molar. 

roots  have  the  same  characteristics  as  the  others  combined  in  the  one 
specimen.  The  diagrams  (Fig.  208)  show  the  scheme  for  the  crown 
and  root. 

Fig.  210  shows  specimens  of  fusion  in  both  the  upper  and  lower 
jaws.      It   occurs    also  with    the    temporary  teeth  (Fig.  211).      Fig. 


222     MALFORMATIOXS  AND  MALPOSITIOXS  OF  THE  TEETH. 

208,  A,  shows  a  very  rare  condition,  the  fusion  of  the  temporary  cen- 
tral, lateral,  and  cuspid  of  one  side  (triple  fusion). 

Fusion  is  evidently  an  abnormality  of  development  dependent  upon 
coalescence  of  formative  organs  at  some  point,  and  is  most  likely  to 
occur  where  the  adjacent  tooth  follicles  have  least  anatomical  sepa- 


FiG.  208. 


Fig.  209. 


A,  diagram  of  a  case  of  triple  fusion  show- 
ing crowns  with  independent  incisal  edges 
and  pulps,  but  otherwise  fused  into  one 
crown  with  one  pulp;  B,  transverse  sec- 
tion of  same,  showing  common  pulp  ca\'ity 
and  common  dentine  overlaid  by  enamel 
(or  cementum).     From  a  specimen. 


Permanent  central  and  lateral  incisors  of  the 
upper  jaw,  united  throughout  the  whole  length  of 
the  teeth.     (Tomes.) 


ration  from  their  fellows.  The  roots 
of  fused  temporary  teeth  are  re- 
sorbed  as  usual  (Fig.  205,  d). 

No    particular    treatment    is    re- 
quired unless  the  mass  in  some  way 
cause    interference    with     function, 
which  is  unusual.    The  teeth  having  a  common  pulp,  no  attempt 
should  be  made  to  divide  them. 

Fusions  are  most  common  between  the  anterior  teeth  of  each  set 
and  between  the  second  and  third  or  third  and  fourth  (supernumerary) 
permanent  molars.  It  has  not  been  noted  in  bicuspids,  presumably 
because  these  teeth  lie  in  the  bifurcations  of  the  temporary  molars. 

Concrescence  of  Teeth.  Concrescence  of  teeth  is  their  union  after 
the  tooth  is  formed;  it  is  evident,  therefore,  that  the  union  can  only  be 
caused  by  fusion  of  cementum.  This  means  that  during  the  formative 
and  eruptive  period  or  after  eruption  the  bony  partition  between  the 
teeth  disappears,  and  that  their  pericementi  become  united,  receding 
from  the  line  of  compression  as  cementum  is  deposited  between  and 
joining  the  roots.  The  united  teeth  show  evidences  of  hypercementosis 
at  points  other  than  the  point  of  union  (Fig.  205,  a,  and  Fig.  212). 

In  the  eruption  of  the  third  molars,  particularly  the  upper,  temporary 
lack  of  space  for  the  eruption  of  the  crown  may  cause  resorption  of 
the  bone  covering  the  roots  of  the  second  molar,  and  fusion  of  the 
formative  pericementum  of  the  third  molar  with  that  of  the  second 
occurs;   a  deposition   of  cementum   then   binds   the   teeth  together, 


MACROSCOPIC  MALFORMA TIONS. 


223 


preventing  the  eruption  of  the  third  molar.  The  lower  third  molar 
rarely  presents  its  roots  to  those  of  the  second  molar;  the  contrary 
presentation  is  the  rule.     The  condition  also  occurs  apart  from  the 


Fig.  210. 


A,  Fusion  of  upper  geminous,  ijermanent  laterals.      B.  Fusion  of  lower  right  permanent 
central  and  lateral  incisors. 


Fig.  211. 


Fusion  of  upper  temporary  teeth.     Double  fusion  of  lower  temporary  lateral  and  cuspid. 

eruptive  process.     Excessive  hypercementosis  upon  the  roots  of  indi- 
vidual teeth  may  finally  result  in  their  union  (Fig.  205,  e). 


Fig.  212. 


224    MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

In  at  least  one  case,  the  crown  of  the  upper  third  molar  was  partly 

erupted  when  concrescence  occurred.     Retained  in  this  situation  the 

crown  decayed  away,  necessitating  extraction;  the 

second  molar  came  away  with  it. 

The  only  treatment  required  for  concrescence  is 
that  indicated  for  hypercementosis  (w^hich  see). 

Gemination  of  Teeth.  (Twin  Teeth.)  This  term 
has  been  used  by  Tomes  in  the  sense  of  union  of 
teeth,  but  it  is  perhaps  better  used  to  designate 
supplemental  teeth  of  the  same  class.  In  twin 
teeth  the  enamel  organ  of  a  permanent  or  temporary 
tooth  is  duplicated,  in  all  probability,  two  buds 
arising  from  the  cord  or  band  as  the  case  may  be. 
One  of  the  teeth  formed  is,  of  course,  a  super- 
numerary tooth,  but  in  some  cases  both  are  typical  teeth  (Fig.  213). 
The  second  germ  may  develop  an  atypical  tooth  or  one  but  slightly 
abnormal  in  form.  The  geminous  teeth  may  undergo  fusion  as  seen 
in  Fig.  210,^4. 

Fig.  213. 


Concrescence.  Third 
upper  molar  impris- 
oned between  the  roots 
of  the  second  molar. 


Double  gemination  of  upper  permanent  lateral  incisors. 

Dilaceration  and  Flexion.  By  dilaceration  is  meant  a  displacement 
of  a  formed  portion  of  a  tooth  in  such  a  manner  as  to  change  its 
relative  position  to  the  soft  parts  engaged  in  its  development,  the 
development  then  being  continued  in  the  new  relation.^  The  term 
"flexion"  may  be  made  to  include  cases  of  abnormal  development 
in  which  the  formative  tissues,  the  enamel  organ,  or  dentinal  papilla 


1  Tonies. 


MACROSCOPIC  MALFORMA TIONS. 


225 


have  had  their  relative  positions  altered  by  unknown  forces.  If,  as  an 
example  of  the  first  class,  an  accident  to  a  temporary  tooth  occur, 
the  force  may  displace  the  partially  formed  permanent  crown.  The 
balance  of  the  crown  may  be  formed  in  the  new  situation  and  be  of 


Fig.  214. 


Fig.  215. 


PC 


PC    BOFR 

Pulp  hernia,  flexion,  and  dilaceration, 
mesodistal  section:  E,  enamel,  distal  section 
in  the  bifurcation  of  the  roots;  I),  dentine; 
C,  C,  cementum;  P  C,  pulp  cavity;  F,  large 
apical  foramen;  B  of  B,  bifurcation  of  the 
roots. 


Dilaceration.   Shows  fold  in  the  labial  enamel  and 
cer^dcal  dentine.      (After  von  Wunschheim.) 


fairly  perfect  or  of  imperfect 
structure.  The  same  is  true  of 
the  tissues  of  the  root;  Fig.  214 
illustrates  both  conditions.^  This 
is  most  likely  to  occur  with  the 
anterior  teeth. 

As  an  example  of  the  second 
class,  a  portion  of  the  enamel 
organ  of  a  tooth  may  be  displaced 
and  in  its  new  relations  may  form  enamel  in  an  unusual  situation,  as, 
for  example,  upon  the  side  or  neck  of  the  root  (see  enamel  nodule)  or 
even  in  the  bifurcation  (Fig.  215).  Again,  it  is  conceivable  that  lack 
of  space  may  cause  deflection  of  a  pulp  engaged  in  root  formation, 
a  curved  root  being  the  result  (Fig.  223). 

Unusual  Locations  of  Enamel.  That  during  development  the  enamel 
organ  or  portions  of  it  may  assume  an  abnormal  relation  to  the  pulp 
is  evidenced  by  odontomes.  Apart  from  these  there  are  evidences 
seen  in  teeth  which  show  that  portions  of  the  enamel  organ  may 
become  detached  from  the  main  organ  and  develop  enamel  in  unusual 
situations.  Thus  columns  of  enamel  may  penetrate  the  body  of  the 
dentine. 

'   G.  von  Wunschheim,  Fracturen,  Infraktionen  und  Knickungen  der  Zahne. 

15 


226     MALFORMATIOXS  AND  MALPOSITIONS  OF  THE  TEETH. 

A  small  nodule  or  cap  of  enamel  overlying  dentine,  and  itself  over- 
lapped at  the  edges  by  cementum,  may  be  found  upon  the  root  of  a 
molar,  usually  upon  the  side  of  an  upper  third  molar  at  a  point  about 
one-eighth  inch  from  the  cervical  margin  of  the  crown  enamel.  A  thin 
ridge  of  enamel  sometimes,  though  not  usually,  seen  connecting  them 
indicates  the  nodule  to  have  been  formed  by  a  detached  portion  of 


Fig.  216. 


Fig.  217. 


Enamel  excrescences. 
(Salter.) 


Lower  molar  with  enamel  nodule  connected  with 
enamel  of  crown  by  a  ridge  of  enamel. 


the  original  enamel  organ.  This  formation  is  known  as  an  enamel 
nodule.  It  may  occur  upon  a  lower  molar,  though  usually  found  upon 
the  upper  molars  (Fig.  217).     They  may  cause  neuralgia  (Ottofy). 

A  molar  root  may  have  a  cap  of  enamel  upon  its  apex,  an  evidence 
of  extreme  displacement.  Sometimes  an  excrescence  may  be  found 
upon  the  enamel  (Fig.  216).  Fig.  215  shows  enamel  formed  in  the 
bifurcation  of  the  roots  of  a  lower  molar. 


Fig.  218. 


Fig.  219. 


Fig.  220. 


Fig.  21S. — Upper  molar  with  supplemental  cusp  on  lingual  side. 

Fig.  219. — Showing  unusual  development  of  the  cingule  or  basal  talon  on  an  incisor. 
case  reported  by  W.  H.  Mitchell,  Dental  Cosmos,  vol.  xxxiv.) 
Fig.  220. — Very  large  supplemental  cusp  on  upper  molar. 


(From 


Supplemental  Cusps.  Occasionally  a  tooth  has  a  greater  number  of 
cusps  than  usual.  The  most  common  form  of  this  condition  is  a 
supplemental  mass  attached  to  the  palatal  side  of  the  mesopalatine 
cone  of  the  upper  first  molars  (Fig.  218).  It  is  more  rarely  the  case 
that  a  cingule  of  this  sort  is  noted  upon  the  lower  molars.  The  palatal 
tubercle,  the  prominence  upon  the  cingule  of  an  upper  incisor,  may 


MACROSCOPIC  MALFORMATIONS. 


227 


be  of  exaggerated  size.  In  one  case  (Fig.  219)  this  development  gave 
the  appearance  of  a  talon  upon  the  tooth,  a  distinct  cusp  segment  in 
itself. 

Fig.  220  ilhistrates  a  marked  supplemental  cusp  upon  the  buccal 
surface  of  a  molar. 

Malformations  of  Roots.  Differences  in  regard  to  the  size,  arrange- 
ment, form,  and  number  of  the  roots  of  teeth  are  the  most  common 


Fig.  221. 


Fig.  222. 


Fig.  223. 


Fig.  224. 


Cuspids  with  long  roots. 


Curved  roots.    Upper  cuspid  with  two  roots.. 


of  dental  malformations.  The  roots  of  teeth  may  be  abnormally  long; 
(Figs.  221  and  222)  or  abnormally  short  (Figs.  225  and  226). 

The  roots  of  cuspids  may  be  bifurcated,  particularly  in  the  lower 
jaw  (Fig.  224). 

The  upper  bicuspids  may  have  bifurcated  roots,  the  extra  root 
usually  being  on  the  buccal  aspect.    The  upper  second  bicuspid  may 


Fig.  225. 


Fig.  226. 


Fig.  227. 


Fig.  225. — Short  buccal  root  of  a  molar,  otherwise  properly  developed. 
Fig.  226. — Central  incisor  with  short  root. 
Fig.  227. — Five-rooted  upper  third  molar. 

be  bifurcated;  upper  molars  may  have  more  than  three  roots,  the 
third  molar  often  having  four,  five,  or  six,  and  in  one  case  reported 
eight  roots  (Fig.  227).  In  some  cases  upper  third  molars  have  but 
one  root  with  a  single,  large  canal.  In  other  cases  the  roots  are  fused 
so  as  to  form  apparently  but  one  root,  while  the  canal  divisions  may 
exist.  Lower  molars  may  have  three  or  four  distinct  roots,  but  at 
times  only  one. 


228     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Abnormalities  of  root  form  are  of  extreme  frequency  and  are  prob- 
ably explained  by  the  hypothesis  of  flexion  of  the  root  pulp,  previous 
to  the  deposition  of  the  curved  portion  of  root  tissue. 


Fig.  228. 


Fig.  229. 


Odontoma.     (Oarretson.) 


Results  of  hernia  of  a  pulp. 

(Salter.) 


It  is  impossible  to  diagnose  the  forms  of  roots  from  the  appearance 
of  the  crowns,  but  an  ic-ray  skiagraph  will  determine  their  form  with 
certainty. 


Fig.  230. 


Fig.  229  magnified. 


Odontomes.  An  odontoma  is  a  growth  composed  of  structures  of 
which  the  teeth  are  composed,  but  the  masses  may  be  so  arranged 
as  to  have  no  typical  form  or  even  resemblance  to  a  tooth.  They  may 
appear  in  the  arch  or  may  remain  embedded  in  the  jaw^  where  they 


MACROSCOPIC  MALFORMA  TIONS. 


229 


may  lie  quiescent  or  may  excite  cyst  formation  (Fig.  27),  or  give  rise 
to  various  morbid  reactions. 

It  has  been  held  by  Broca  that  any  of  the  formative  organs  of  the 
tooth — enamel  organ,  dentinal  papilla,  or  follicular  wall — may  undergo 
aberrant  development  and  may  there- 
after deposit  calcific  tissue  or  not,  as  Fig.  231. 
the  case  may  be.     If  not,  tumors  not 
distinctly  dental  may  form. 

Figs.  229,  230,  and  231  illustrate 
odontomes  of  simple  and  self -explain- 
able nature.  After  completion  of  a 
crown  and  portion  of  the  roots  the 
pulp  has  suddenly  enlarged  far  be- 
yond its  typical  form,  carrying  with  it  the  follicular  wall.  Ceasing  to 
enlarge,  deposition  of  dentine  has  taken  place  at  the  expense  of  the  pulp. 

Over  this  dentine  the  follicular  wall  has  deposited  cementum.  The 
whole  forms  what  has  been  called  a  radicular  odontome.  The  expansion 
of  the  pulp  has  been  termed  a  pulp  hernia.     (See  also  Fig.  215.) 


Results  of  pulp  hernia.     (Tomes.) 


Fig.  232. 


Extreme  malposition  of  molar  germs.     (From  model  in  Philadelphia  Academy  of  Stomatology.) 


The  diagnosis  of  the  presence  of  odontomes  in  cases  of  tumor 
formation  is  made  either  visually,  by  .r-rays,  or  by  incision  and  explo- 
ration.   The  treatment  consists  of  their  removal  by  surgical  operation. 

Fig.  232  illustrates  a  case  which  is  probably  merely  a  case  of  abnor- 
mal molar  germs  which,  after  misplacement  in  some  manner,  have 
developed  in  the  incisal  region  and  pushed  aside  the  central  incisors. 


230      MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Anomalies  of  Number.  Although  the  dental  series  of  man  normally 
consists  of  thirty-two  members,  cases  are  frequently  observed  in  which 
the  number  is  less  than  or  in  excess  of  that  number. 

Deficiency.  It  is  observed  with  some  frequency  that  the  upper 
lateral  incisors  never  make  their  appearance,  a  condition  traceable  to 
the  influence  of  heredity  in  some  of  the  instances.  In  an  interesting 
case  of  three  sisters,  who  all  were  without  upper  laterals,  a  son  of  one 
of  them  had  them.  Unfortunately  the  history  as  to  the  parents  of 
the  sisters  was  not  certain,  as  they  wore  artificial  teeth. 

When  the  laterals  are  absent  the  permanent  cuspid  erupts  and 
occupies  the  lateral  incisor  space,  and  thus  sometimes  fails  to  cause 
resorption  of  the  root  of  the  temporary  cuspid,  which  persists  in  the 
cuspid  space  (Fig.  179).  The  lower  laterals  sometimes,  but  more 
rarely,  fail  to  appear;  are  probably  never  formed.  The  third  molar 
may  never  appear  or  appear  as  a  peg-like  tooth. 

The  cases  of  suppressed  teeth  next  in  point  of  frequency  are  those 
of  the  bicuspid  teeth.  If  the  corresponding  teeth  are  all  present  in 
the  dental  arch,  a  well-founded  suspicion  of  impaction  of  the  missing 
tooth  may  be  entertained. 

An  excessive  growth  of  hair  upon  the  face  and  body  has  also  been 
associated  in  some  cases  wath  a  deficiency  in  number  and  alteration 
in  form  of  the  teeth.  In  other  cases  no  abnormality  was  noticeable.^ 
In  some  cases  the  hair  and  other  dermal  structures  may  be  normal 
and  the  teeth  be  quite  deficient  in  number. 

The  extreme  of  suppressed  formation  is  represented  in  a  case 
described  by  Guilford.^ 

A  patient  over  fifty  years  old  had  never  erupted  any  teeth,  temporary 
or  permanent;  the  alveolar  arches  revealed  no  e\'idences  of  enclosed 
teeth,  but  had  the  appearance  of  typical  edentulous  jaws;  the  alveolar 
bone  itself  was  but  primitive.  The  case  appeared  to  be  sporadically 
hereditary,  a  grandparent  and  an  uncle  exhibiting  a  like  condition. 
The  cases  are  interesting  also  because  of  additional  evidences  of  faulty 
evolution  of  dermoid  structures.  In  the  first  case  cited  no  sudoriparous 
glands  appear  to  have  formed,  and  there  was  but  a  faint  growth  of 
hair  on  the  cranium,  and  none  on  the  face  and  body.  The  uncle  was 
hairless  and  edentulous  from  birth.  Guilford  found  in  other  members 
of  the  family  an  absence  of  the  full  complement  of  teeth. 

Excess.  The  possible  occurrence  of  a  condition  in  some  respects 
the  reverse  of  the  preceding  has  been  much  written  of  and  discussed 

^  Tomes.  2  American  System  of  Dentistry,  vol.  iii. 


ANOMALIES  OF  NUMBER.  231 

— i.  e.,  the  occurrence  of  a  complete  third  denture.  There  can  be  but 
one  conclusion  from  an  examination  of  all  the  evidence  thus  far 
presented,  and  that  is  that  no  clear  and  well-authenticated  cases  are 
made  out.  Isolated  cases  of  the  appearance  of  teeth  subsequent  to 
the  loss  of  all  of  the  second  denture  are  not  infrequent;  and,  so  far  as 
clear  records  can  be  obtained,  are  resolvable  into  cases  of  the  eruption 
of  supernumerary  or  impacted  teeth.  While  these  cases  are,  at  least  for 
the  present,  to  be  held  as  unproved  in  connection  with  elderly  per- 
sons, a  well-authenticated  case  of  multiple  dentition  in  a  child  is 
recorded  'by  Catching.^  Between  the  sixth  and  seventh  month  the 
eruption  of  one  set  of  teeth  was  complete;  within  three  months  all  of 
these  had  been  lost.  Between  the  eleventh  and  fifteenth  months 
another  period  of  dentition  occurred,  the  teeth  of  this  second  denture 
being  of  such  faulty  structure  as  to  crumble  away  quickly.  At  the 
age  of  two  and  one-half  years  a  third  dentition  appeared,  which  caused 
the  child  such  inconvenience  that  the  teeth  were  extracted  by  the 
mother.  At  the  age  of  eleven  years  a  fourth  series  erupted,  incom- 
plete through  the  absence  of  six  teeth.  At  the  age  of  fifteen  these 
teeth  were  sound  and  firm. 

Fourth  Molar.  The  molar  series  of  man,  particularly  in  the  lower 
negroid  races,  may  consist  of  four  instead  of  three  members.  When 
the  fourth  molar  appears  in  the  white  races  it  is  usually  as  a  stunted 
member,  a  conical  or  peg-like  tooth,  similar  to  that  which  occasionally 
replaces  the  third  molar.  There  is  rarely  room  posterior  to  the  distal 
wall  of  the  third  molar  for  their  eruption,  so  that  they  make  their 
appearance  in  the  region  shown  in  the  illustration.  S.  M.  Hartman,^ 
L.D.S.,  of  Victoria,  B.  C,  has  furnished  the  model  (Fig.  233)  of  a 
case  in  which  the  molar  form  of  the  fourth  tooth  is  unusually  well 
pronounced. 

Supernumeraxy  Teeth.  Any  teeth  in  excess  of  the  normal  thirty- 
two,  although  clearly  cases  of  reversion  of  type  in  many  instances,® 
are  included  in  the  category  of  supernumerary  teeth.  Supernumerary 
teeth  appear  as  simple  unmodified  cones,  or  as  combinations  of  cones 
resembling  the  forms  of  teeth.  The  conical  form  is  most  common. 
Cases  where  these  peg-like  teeth  appear  around  the  third  molars 
singly  or  in  number  are  numerous.  Their  appearance  in  any  situa- 
tion is  evidence  that  the  normal  number  of  dental  cords  has  been 


1  Southern  Dental  Journal,  October,  1886.  2  Dental  Cosmos,  1891. 

^  A.  H.  Thompson,  American  System  of  Dentistry,  vol.  iii.,  and  American  Text-book  of 
Operative  Dentistry. 


232     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

exceeded.  They  are  perliaps  all  to  be  regarded  as  cases  of  long  rever- 
sion, not  alone  because  they  increase  the  number  of  the  dental  series, 
but  because  they  have  primitive  forms,  a  modification  of  the  forms 
found  among  the  reptiles  and  fishes. 


The  fourth  molar.     (Hartman.) 
Fig.  2.34. 


Two  atypical  upper  .supernumerary  teeth  displacing  the  incisors. 

Guilford^  divides  supernumerary  teeth  into  those  having   typical 
anatomical  forms  and  those  ha\dng  the  atypical  forms. 

1  American  System  of  Dentistry,  vol.  iii. 


MALPOSITIONS  OF  THE  TEETH.  233 

Supernumerary  incisors  having  typical  forms  appear  in  either  jaw. 
In  the  upper  jaw  supernumerary  centrals  and  laterals  both  appear, 
the  latter  more  frequently  (Fig.  213).  Supernumerary  teeth  may 
occupy  any  position  relative  to  the  dental  arch,  but  are  more  frequently 
seen  at  its  lingual  side.  The  compound  cone  occasionally  appears 
(Fig.  236).  In  addition  to  molars  and  incisors,  supernumerary 
bicuspids  are  occasionally  found  (Fig.  235);  supernumerary  cuspids 
are  very  rare,  but  sometimes  a  brood  of  them  exists,  as  many  as  seven- 
teen fairly  defined  small  teeth  having  been  removed  from  a  cyst  in  the 
location  of  the  cuspid  tooth. ^ 

Fig.  235. 


Case  of  seven  lower  bicuspids,  two  supernumeraries  in  place  and  one  erupting.  This  patient 
has  two  supernumerary  upper  central  incisors  displacing  the  centrals  proper,  yet  closely 
resembling  them. 

Unless  supernumerary  teeth  are  a  source  of  offence,  either  through 
their  position  or  appearance,  they  need  not  be  disturbed.  If  they 
are  found  to  be  so,  they  may  be  extracted. 

Malpositions  of  the  Teeth.  A  tooth  is  said  to  be  in  malposition 
when  it  is  not  in  normal  relation  with  the  dental  arch  to  which  it 
belongs  and  to  its  antagonizing  teeth  of  the  opposing  arch.  Teeth  are 
found  in  abnormal  positions  as  the  result  of  a  variety  of  causes.  Some 
of  these  operate  prior  to,  during,  or  immediately  after  eruption;  some 
long  after  the  eruption  of  the  teeth,  and  some  because  of  non-eruption 
of  teeth. 

Malpositions    which    are   remediable   through   the    application   of 

'  D.  M.  Clapp,  International  Dental  Journal,  1900. 


234    MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

mechanical  force  applied  by  means  of  suitable  apparatus  belong  to 
operative  dentistry,  as  has  been  stated.    They  are  fully  treated  of  in 
works  upon  operative  dentistry^  and  orthodontia,"  so  that  their  dis- 
cussion in  a  treatise  upon  pathology  might  seem  a  work  of  super- 
erogation; the  plan  of  the  book,  however,  demands  their  brief  mention. 
Malposed  teeth  may  occupy  any  position  relative  to  the  dental  arch, 
and  any  teeth  of  the  dental  series  may  be  the  offenders,  although  most 
commonly  noted  in  connection  with  the  incisors.    So  common  is  some 
degree  of  irregularity  of  the  position  of  the  lower  incisors  that  its 
appearance  is  scarcely  regarded  as  abnormal.     The  teeth  may  be 
inside  or  outside  the  dental  arch,  or  have  their  trans- 
verse axes  at  any  angle  with  the  arch  line — i.  e.,  may  be 
rotated  in  any  manner.     In  the  most  aggravated  cases 
an  entire  half  denture  may  be  malposed  as  regards  its 
relations  with  the  opposing  or  antagonizing  half.    In- 
stead of  having  the  upper  teeth  occluding  outside  the 
lower,  they  may    occlude   inside.      They  may   occlude 
squarely  without  incisor  overlapping.      Both  of   these 
abnormal  conditions  are,  of  course,  due  to  lack  of    correspondence 
between  the  development  of  the  lower  and  upper  jaws.     If  one  jaw 
has  developed  normally,  the  other  has  necessarily  developed  insuffi- 
ciently or  too  much. 

Causes  of  Malposition.  Individual  teeth  become  malposed  at  times 
through  injudicious  extraction  of  temporary  teeth.  The  extraction 
of  a  second  temporary  molar  may,  for  example,  permit  the  approx- 
imation of  the  first  permanent  molar  and  the  first  bicuspid  and  the 
second  bicuspid  be  thus  compelled  to  either  the  buccal  or  the  lingual 
side.  Lack  of  space  in  the  bicuspid  region  may  compel  these  teeth 
to  the  lingual  side,  producing  what  is  termed  a  saddle-shaped  arch. 

Such  lack  of  space  for  the  accommodation  of  teeth  may  thus  be 
due  to  movement  of  the  other  teeth,  to  a  lack  of  correspondence  in 
the  size  of  the  teeth  and  jaw,  or  to  arrested  development  of  the  jaw. 

The  injudicious  retention  of  a  temporary  tooth  root  may  cause  the 
deflection  of  a  permanent  tooth. 

If  adenoids  or  nasal  polypi  exist  the  child  may  become  a  mouth 
breather,  a  habit  wliich  causes  the  muscles  to  compress  the  sides  of 
the  teeth  and  alveolar  arches.  As  a  result  the  arch  is  flattened  on  the 
sides  and  pointed  anteriorly.    The  deformity  is  known  as  the  V-shaped 

1  American  Text-book  of  Operative  Dentistry. 
-  Giiilford,  Angle,  and  others. 


IMPACTION  AND  ENCYSTMENT.  235 

arch.  Habits  such  as  thumb  or  Hp  sucking  are  frequent  causes  of 
protrusion  of  the  upper  anterior  teeth.  Excessive  or  defective  develop- 
ment of  the  upper  or  lower  jaw,  wholly  or  in  part,  produces  a  lack  of 
correspondence  in  the  two  arches.  Thus  there  may  be  inferior  or 
superior  protrusion  or  retrusion.  It  has  been  pointed 
out  by  Talbot  that  constitutional  conditions  are  re- 
sponsible for  arrested  or  excessive  developments  of 
portions  of  the  body. 

If  the  first  permanent  molars  be  extracted  before 
the  bicuspids  are  erupted,  the  occlusion  does  not 
deepen  normally.  The  lower  incisors,  erupting  early? 
come  to  strike  the  uppers  at  their  linguocervical  por- 
tions, driving  them  forward  (Fig.  237).  To  avoid  this 
the  first  molars  should  be  retained  as  props,  even  if 
only  temporarily  until  the  bicuspids  are  in  position.  Effects  of  prema- 

The  first  molars  are  the  keystones  of  the  arches    *"""  ^°''  °^  p^"""^^" 

''  nent  first  molars. 

and  determine  the  extent  of  the  formative  process 
which  shall  occur  in  the  alveolar  bone  posterior  to  them.     They  are 
also  the  teeth  which,  correctly  placed  or  out  of  position,  determine 
the  occlusion  of  the  teeth. ^ 

If  a  temporary  tooth  be  long  retained  it  is  sometimes  raised  to  the 
occlusal  level  of  the  other  teeth;  again,  it  is  sometimes  left  at  its  original 
level  and  occasionally  imprisoned  between  other  teeth.  The  a:-ray 
should  be  used  to  determine  the  presence  or  absence  of  the  permanent 
tooth  germ  or  resorption  of  the  temporary  roots  (Fig.  175). 

If  teeth  erupt  in  malposition  it  is  held  as  wise  to  correct  as  early 
as  possible,  in  order  to  prevent  further  malposition  of  other  teeth. 

Impacted  and  Encysted  Teeth.  The  extreme  extent  of  dental 
malposition  is  reached  when  the  permanent  teeth  do  not  erupt  at  all. 
Instead  of  presenting  in  the  dental  arch,  they  may  be  entirely  embedded 
in  the  substance  of  the  bone,  either  remaining  there,  with  or  without 
pathological  manifestations,  or  erupting  in  some  very  unusual  situation. 
In  other  cases  a  distinct  cystic  tumor  forms  about  the  enclosed  tooth 
{Fig.  27). 

Impacted  Lower  Third  Molars.  By  far  the  most  common  dental 
impaction  is  that  of  the  lower  third  molar.  The  extent  of  impaction 
varies  from  a  partial  eruption,  or  partial  imprisonment  of  the  tootJi  by 
its  bony  surroundings,  to  its  entire  imprisonment  in  any  part  of  the 
ramus.     Many  of  the  more  severe  cases  treated  of  under  the  head  of 

1  Angle. 


236     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

difficult  eruption,  if  unrelieveil,  would  be  included  in  the  category  of 
impacted  teeth. 

In  Fig.  238  is  shown  a  lower  third  molar  presenting  the  effects  of  a 
previous  impaction.  The  irritation  caused  by  the  efforts  of  the  tooth  to 
disengage  itself  or  to  overcome  the  resistance  to  its  eruption  has  caused 
an  active  formative  reaction  in  the  pericementum,  resulting  in  a  hyper- 
trophy of  the  cementum. 

If  the  distance  between  the  posterior  surface  of  the  second  molar 
and  the  columns  of  the  coronoid  process  be  very  short,  it  is  evident  that 
upward  eruption  is  impossible,  so  that  the  tooth  may  assume  any 
direction  of  movement,  the  most  common  being  forward,  the  axis  of 
the  tooth  changing  its  position  until  the  tooth  may  lie  in  a  horizontal 
position  or  even  become  inverted. 

Fig.  238. 


Right  half  of  lower  jaw,  showing  an  impacted  third  molar.      (Cryer.) 


Fig.  239  is  taken  from  the  same  jaw  as  Fig.  238,  but  shows  the 
opposite  side;  the  impaction  is  pronounced.  Fig.  240  shows  another 
case  with  different  anatomical  surroundings.  In  the  first  case  there 
were  evidences  both  in  the  tooth,  in  its  bony  surroundings,  and  in 
the  external  cortical  bone,  of  the  results  of  the  irritation  produced  by 
the  efforts  at  eruption.  The  cementum  was  thickened;  the  outer 
follicular  wall,  the  tissue  designed  to  form  the  alveolar  periosteum,  had 
exercised  its  formative  osteogenetic  function,  and  a  capsule  of  bone  had 
formed  about  the  tooth;  it  lay  in  a  bony  chamber.  The  pressure 
exerted  upon  the  distal  wall  of  the  second  molar  had  resulted  in  a 
pressure  resorption  of  its  root  until  the  pulp  chamber  was  encroached 


IMPACTION  AND  ENCYSTMENT. 


237 


upon.  In  Fig.  240  the  root  development  has  caused  impingement  of 
the  root  apex  upon  the  inferior  dental  canal.  These  were  both  post- 
mortem cases,  and  no  records  of  their  clinical  histories  were  obtainable. 
The  symptoms  produced  could  only  be  surmised  by  the  nature  of  the 
anatomical  relations  and  the  pathological  evidences.  There  may  have 
been  a  prolonged  but  mild  periostitis,  probably  a  continued  pulp 
irritation;  and  in  the  last,  neuralgia  of  any  grade  of  severity. 


Fig.  239. 


Inner  side  of  left  half  of  same  lower  jaw.     (Cryer.) 
Fig.  240. 


Impaction  ofjlower  third  molar.     Resorption^of  root  of  second  molar  and  impingement  of  root 
upon  inferior  dental  canal,      (Cryer.) 


238     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

Judging  from  post-mortem  records,  cases  of  impacted  third  molars 
are  more  common  than  generally  believed.  Instead  of  remaining  in 
the  alveolar  portion  of  the  bone,  the  impacted  tooth  may  come  to 
occupy  a  cavity  in  some  portion  of  the  body  or  tlie  ramus  of  the  bone 
(Figs.  242  and  243).    The  positions  of  the  teeth  in  such  cases  tend  to 


Fig.  241. 


-  -h.jwn  in  Fig.  239  with  tooth  remo\  t  i.       '  : .  '-i.) 


Fig.  242. 


Wisdom  teeth  embedded  in  the  rami  of  the  lower  jaw.     (Tomes.) 

confirm  Tomes'  theory  of  the  development  of  the  jaw.  The  jaw  being 
lengthened,  and  the  ramus  developing  through  conjoined  deposition  and 
resorption  of  bone,  the  crown  of  the  tooth  appears  to  be  either  fixed  in 
a  bony  nucleus  and  transported  to  some  distant  point  in  the  develop- 
mental progress  of  the  jaw,  or  to  be  irregularly  shifted  about  during 
jaw  growth.    At  later  periods  the  pressure  exercised  by  root  formation 


IMPACTION  AND  ENCYSTMENT. 


239 


Ftg.  243. 


disturbs  the  relations  of  the  tooth  with  its  earher  surroundings.  These 
efforts  at  eruption  may  at  late  periods  cause  the  appearance  of  the 
tooth  in  odd  situations.  In  the  case  shown  in  Fig.  244  the  crown  of 
the  tooth  made  its  way  through  the  angle  of  the  bone  and  through  the 
muscles  and  skin.  The  opening  in 
the  skin  healed  upon  extraction  of 
the  tooth. 

Impacted  Upper  Third  Molars. 
Some  phases  of  impaction  of  this 
tooth  have  been  spoken  of  under 
the  head  of  difficult  dentition.  The 
most  common  is  imprisonment  of 
the  tooth  and  its  subsequent  partial 
eruption  in  a  horizontal  position,  the 
crown  pointing  toward  the  cheek 
(Fig.  245).  The  crown  of  this  tooth 
may  in  rare  cases  be  directed  in- 
ward or  backward,  in  the  latter  case 
being  arrested  by  the  pterygoid 
plates  of  the  sphenoid  bone. 

In  a  case  recorded  by  Tomes  (Fig. 
246)    the  extraction  of   the  second 
molar  revealed  the  third  molar  in  a  reversed  position,  its  roots  occupy- 
ing the  depression  between  the  roots  of  the  second  molar. 

Impacted  Cuspids.     In  point  of  frequency  of  impaction  the  upper 
cuspids  stand  next  to  the  lower  third  molars.    It  will  be  recalled  that 


Wisdom  tooth  buried  in  the  ramus. 
(Tomes,  after  Marshall.) 


Fig.  244. 


From  a  wax  model  in  the  museum  of  the  London  Odontological  Society.     (Tomes.) 


the  upper  cuspids  lie  high  up;  the  floors  of  their  crypts,  in  which  they 
lie  loosely,  are  at  a  higher  level  than  those  of  the  adjoining  teeth;  they 
erupt  at  a  much  later  period,  and  their  crowns,  as  with  the  other 


240     MALFOmfATIONS  AND  MALPOSITIOXS  OF  THE  TEETH. 


anterior  teeth,  lie  lingual  to  the  roots  of  their  predecessors.  All  of  these 
are  elements  which  might  cause  displacement  of  the  developing  cuspids. 
Should  the  advance  of  eruption  not  keep  pace  with  the  development 
of  the  alveolar  bone,  imprisoinnent  is  likely;  again,  the  dense  bone 


Fig.  245. 


Fi(i.  2-ir>. 


A  second  molar  of  the  upper  jaw,  with  the 
wisdom  tooth  inverted  and  embraced  within 
the  roots.     (Tomes.) 


Upper  jaw,  with  the  third  molar  directed 
forward,  and  impinging  upon  the  second  molar. 
The  small  tooth  situated  high  up  in  the  ante- 
rior part  of  the  jaw  was  forced  there  by  the 
spade  of  the  grave-digger.  The  artist's  accu- 
racy in  delineating  all  parts  of  the  specimen 
has  rendered  this  explanation  necessary. 
(Tomes.) 


immediately  about  the  first  bicus- 
pid and  lateral  incisor  may  offer  a 
deflecting  resistance.  Examining 
the  texture  of  the  bone  about 
these  parts,  it  is  evident  that  the 
direction  of  least  resistance  to  the  advance  of  a  much  deflected  crown 
is  into  the  cancellated  bone  of   the   incisor  portion  of  the  alveolar 

Fig.  247. 


-Abnormal  jaw,  showing  impacted  cuspids.      (Cryer.) 

process;  hence  it  is  most  usual  to  find  the  crowns  of  these  teeth  lying 
with  their  cusps  pointing  forward  (Fig.  247).  Several  recorded  cases 
have  the  positions  shown;  one  or  both  of  the  teeth  may  be  impacted. 


IMPACTION  AND  ENCYSTMENT. 


241 


Cuspid  teeth  may  erupt  into  the  nasal  cavity,  appear  in  the  canine 
fossa  and  present  the  crowns  cheekwise  or  He  horizontally  and  above 
the  roots  of  the  bicuspids. 


Fig.  248. 


Impacted  bicuspid.     (Salter.) 
Fig.  249. 


Imprisoned  central  incisor.      (Kirk  and  Cryer.) 


Impaction  of  Other  Teeth.  While  impactions  are  most  common  in 
connection  with  the  teeth  named,  any  other  teeth  of  a  denture  may 
be  imprisoned.  Fig.  248  shows  an  impacted  bicuspid  whose  root 
development  has  been  normal  as  regards  its  length,  but  whose  curve 
has  been  modified  by  the  resistance  of  surrounding  tissues.  Fig.  249 
exhibits  an  imprisoned  central  incisor,  whose  retention  was,  no  doubt, 

16 


242     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

determined  and  malposition  caused  by  the  development  and  presence 
of  the  brood  of  supernumerary  teeth  which  surround  its  crown. 

Upper  incisor  teeth  have  been  seen  inverted  and  their  crowns 
erupted  into  the  nasal  cavity,  where  they  have  produced  inflammation 
which  later  became  infective/ 

Symptoms.  The  most  common  symptom  attendant  upon  impaction 
of  teeth,  judging  from  the  obtainable  records  of  cases,  is  trifacial 

Fig.  250. 


Lower  maxilla,  in  which  the  right  second  bicuspid  is  placed  obliquely,  the  root  being  directed 
backward.  The  crown,  though  exposed,  does  not  rise  above  the  level  of  the  alveolar  margin. 
(Tomes.) 

Fig.  251. 


Maxilla,  in  which  the  temporary  cuspids  (the  sockets  of  which  are  shown  by  the  dotted  lines) 
were  retained,  and  the  permanent  canines  developed  within  the  substance  of  the  jaw.  The 
bone  has  been  removed  on  the  one  side  to  show  the  direction  taken  by  the  tooth,  which  has 
been  twisted  on  its  axis  to  the  extent  of  a  quarter  of  a  turn.     (Tomes.) 

neuralgia  of  any  degree,  caused  by  impingement  of  the  malposed  tooth 
upon  nerve  filaments  or  trunks.  Cryer  records  a  case  where  a  supra- 
maxillary  neuralgia  was  traced  to  the  presence  of  a  central  and  lateral 
incisor,  and  a  cuspid  tooth  in  the  anterior  wall  of  the  antrum;  /they 
were  only  discovered  by  an  exploratory  operation  (Fig.  252).  A  cure 
of  the  neuralgia  was  effected  by  their  removal. 

1  Jameson,  International  Dental  Journal,  1899.  ^  Dental  Cosmos,  1896. 


IMPACTION  AND  ENCYSTMENT.  243 

Impacted  third  molars  frequently  give  rise  to  heavy  rheumatic  pains 
about  the  side  of  the  face  and  jaws,  and  no  doubt  in  such  cases  as 
depicted  in  Fig.  240  would  cause  intractable  and  diffuse  maxillary 
neuralgia.  Salter^  records  a  case  of  long  standing  and  intractable 
neuralgia,  exhibiting  a  constant  painful  area 
upon  the  scalp,  and  in  which  heat  and  tender- 
ness were  noticed  over  a  swelling  upon  the 
hard  palate.  Immediate  and  permanent  ces- 
sation of  the  neuralgia  followed  removal  of 
the  teeth. 

Symptoms  of  maxillary  periostitis — heavy, 
gnawing,  and  dull,  throbbing  pain,  with  more  or  less  heat  and  en- 
gorgement of  tissues — are  noted  as  an  accompaniment  of  impacted 
teeth.  Such  symptoms  may  herald  the  appearance  of  the  tip  of  the 
tooth  through  its  bony  covering  and  gum. 

Cases  of  maxillary  abscess,  in  the  absence  of  their  usual  cause 
(gangrenous  pulp),  may  run  a  prolonged  and  painful  course,^  involving 
neighboring  structures,  and  after  free  venting  be  found  to  have  arisen 
about  an  impacted  tooth. 

Occasionally  a  circumscribed  swelling  is  noted  upon  some  aspect  of 
a  jaw,  most  frequently  upon  the  palatal  portion  of  the  superior  maxilla, 
which  is  attended  by  inflammatory  symptoms,  and  an  incision  reveals 
an  impacted  tooth. 

Quickly  forming  cysts  of  the  jaw,  upon  receiving  surgical  treatment, 
may  be  found  to  contain  the  crown  of  an  entire  tooth,  this  evidently 
being  the  centre  of  irritation  from  which  the  cystic  formation  had  its 
origin. 

The  pulps  of  other  teeth  have  been  devitalized  by  the  strangulation 
due  to  the  pressure  of  the  crown  of  the  impacted  tooth  upon  the 
apical  tissue. 

The  resorption  of  roots  of  other  teeth  has  been  produced  by  the 
pressure  of  the  impacted  tooth. 

Hypercementosis  and  concrescence  have  also  been  produced  by  the 
descent  of  the  tooth  and  has  produced  impaction.     (See  p.  222.) 

In  all  these  cases  diagnostic  features  exist,  though  none  are  com- 
parable to  the  x-rajs. 

Diagnosis.  The  first  point  of  observance  in  cases  of  suspected 
tooth  encystment  is  an  examination  of  the  dental  arches.  Are  all  of 
the  permanent  teeth  in  position?    Given  the  absence  of,  particularly, 

1  Dental  Pathology.  -  See  Garretson's  Oral  Surgery  and  Salter's  Dental  Pathology. 


244    MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH. 

a  lower  third  molar  from  the  dental  arch,  with  a  history  of  no  eruption, 
and  a  persistent  neuralgia,  particularly  if  occasionally  accompanied  by 
or  alternated  with  heavy  rheumatic  or  what  are  known  as  bone 
pains,  and  finding  no  other  evident  cause  of  the  neuralgia,  an 
impacted  tooth  would  be  naturally  diagnosed  as  the  source  of  the 
disturbance.  Impacted  teeth  which  lie  horizontally,  or  nearly  so,  along 
the  palatal  vault  frequently  cause  a  swelling.  This,  taken  in  con- 
junction with  the  absence  of  a  tooth  from  the  dental  arch,  points  to 
a  diagnosis  of  impaction. 

In  very  many  cases  of  impaction  diagnosis  has  been  a  mere  accident, 
discovery  being  made  in  the  course  of  an  exploratory  surgical  oper- 
ation. Modern  science  solves  with  the  .r-ray  the  difficulties  attendant 
upon  the  diagnosis  of  impacted  teeth.  B.  H.  Catching^  was  the  first 
to  practically  apply  this  diagnostic  test  in  this  connection.  The  left 
upper  central  incisor  of  a  female,  aged  nineteen  years,  became 
loosened,  and  an  exploration  through  its  pulp  chamber  revealed  a 
hard  body  occupying  a  position  part  way  up  the  root,  which  had 
undergone  resorption  to  that  point.  The  cus- 
FiG.  253.  p- J  q£  ^j^g  jg£^  g-^g  ^^,^g  absent  from  the  arch. 

A  skiagraph  of  the  parts  (Fig.  253)  revealed 
the  missing  cuspid,  wdiose  crown  had  impinged 
upon  and  caused  resorption  of  the  root  of  the 
central  incisor. 

Impacted  teeth  may  become  uncovered  at 
some  aspect  late  in  life  and  the  condition  be 
discovered   incidentally.      Cases    are    recorded 

X-ray  photograph,  show-         i  j.i  p  i    j       i  i    xi 

ing  the  maiposed  cuspid  ^hcre  the  pressure  of  a  plate  has  caused  the 
entirely  embedded  in  the    rcsorptiou    of    tissucs   ovcrlyiug    an    impacted 

bone,  and  pressing  upon  the  , .  .  _,.  _ 

central.  tooth,  thus    rcvcalmg   its    presence.     Fig.    254 

illustrates  a  case  w^here  the  presence  of  an  im- 
pacted cuspid  was  revealed  at  the  age  of  seventy  years,  through 
resorption  of  the  alveolar  bone  and  the  gum  tissue  covering  the 
tooth. 

As  the  smooth  feel  of  enamel  is  a  diagnostic  feature  when  instru- 
mental examination  is  made,  it  is  to  be  remembered  that  the  enamel 
and  dentine  of  an  impacted  tooth  may  undergo  a  true  resorption 
with  the  characteristic  Howship's  lacunse.  When  partly  exposed  to 
the  oral  fluid  caries  may  occur.  Both  these  conditions  produce  rough 
surfaces. 

1  Catching's  Compend,  1896. 


IMPACTION  AND  EXCYSTMENT. 


245 


Treatment.  The  treatment  of  cases  of  impaction  is  the  removal 
of  the  offending  tooth.  ^Vhether  or  not  this  comes  within  the  province 
of  the  dental  operator  depends  upon  the  position  of  the  tooth,  and, 
incidentally,  upon  the  usual  range  of  practice  of  that  particular  prac- 
titioner. When  the  tooth  is  embedded  deep  in  the  substance  of  the 
jaw,  access  to  it  involves  the  etherization  of  the  patient  and  the  removal 
of   the   bone  which  obstructs  the 

path  of    extraction;   this  may  be  ^^*^-  ^^*- 

an  operation  of  some  magnitude, 
and  is  usually  done  by  a  special 
surgical  practitioner.  When,  how- 
ever, it  is  evident  that  the  ob- 
structions to  the  removal  of  the 
tooth  consist  of  the  soft  tissues 
and  but  a  lamina  of  bone,  the 
operation  for  removal  is  clearly 
within  the  province  of  the  dental 
operator.  For  example,  the  pres- 
ence of  an  impacted  cuspid  is  de- 
termined lying  horizontally  along 

the  lateral  aspect  of  the  roof  of  the  mouth.  The  parts  may  be  injected 
with  a  cocaine  or  eucaine  solution,  and  a  curv^ed  cut  made  mth  a 
sharp  bistoury  through  the  soft  tissues  at  the  dental  side  of  the 
swelling  to  the  bone.  The  flap  thus  outlined  is  raised  from  the  bone, 
the  flap  including  the  periosteum.  A  large,  sharp  bur  is  then  em- 
ployed to  remove  the  covering  bone.  When  the  tooth  is  freely  ex- 
posed it  may  be  dislodged  with  forceps  or  elevator.  The  parts  are 
then  washed  with  a  hydrogen-dioxide  solution,  dried,  the  flap  pressed 
back  into  place,  and  steresoP  painted  over  the  parts. 


Impacted  cuspid  revealed  by  resorption  of  the 
overlsdng  tissues.    (Burdach.) 


1    R- 


-Purified  gum  lac. 

., 

Six. 

Purified  gum  benzoin, 

S'/3 

Balsam  of  tolu, 

S'/3 

OU  of  cinnamon 

(Chinese), 

Jl/j. 

Acid,  carbolic, 

Siij. 

Saccharin, 

S'/5 

Alcohol, 

Oij.- 

-M.     (BerUoz.) 
—Dental  Cosmos,  1895. 

SECTION  III. 

AFFECTIONS  OF  THE  ENAMEL  AND  DENTINE. 


CHAPTER   X. 

ABRASION,  EEOSION,  AND  STAINS. 

MECHANICAL  INJURY  OF  THE  TEETH. 

Formed  by  the  ameloblasts,  later  changed  into  Nasmyth's  membrane, 
and  borne  upward  with  the  crown  during  the  process  of  eruption, 
enamel  has  no  posteruptive  source  of  nutritive  supply  from  without. 

Its  only  conjectural  source  of  nutrition  is  therefore  from  the  pulp 
via  the  dentinal  tubuli.  Of  this  there  is  no  positive  proof  beyond 
that  offered  by  Caush.  (See  p.  141.)  Teeth  do  change  in  color  with 
advancing  age,  but  this  is  probably  due  to  changes  in  the  color  of  the 
dentine  transmitted  through  enamel,  which  is  normally  almost  or 
even  quite  transparent.  Such  a  transparency  may  be  seen  at  the 
incisal  edges  of  thin  incisors  before  these  edges  are  worn  down. 
Another  proof  of  transmission  of  color  through  enamel  is  seen  in 
caries;  a  bluish-black  or  white  appearance  is  caused  by  the  decayed 
mass  or  decalcified  inner  surface  of  the  enamel. 

Again,  amalgam  or  gold,  oxyphosphate  or  oxychloride,  reflects  its 
color  through  enamel,  and  in  excavating  the  shadow  of  the  excavator 
may  be  seen  through  thin  walls.  Enamel  may  be  stained  or  whitened 
by  decalcification  due  to  causes  acting  externally.  Extreme  polishing 
may  also  cause  a  new  character  of  light  reflection  simulating  a  change 
in  color. 

After  implantation  a  tooth  may  somewhat  change  its  color,  but  this 
evidently  cannot  be  due  to  nutrition  from  the  pulp,  as  this  organ 
will  have  been  removed  before  implantation. 

It  is  generally  regarded  as  a  fact  that  while  enamel  may  suffer 
mechanical  and  chemical  injury  it  undergoes  no  constructive  changes 
or  retrograde  metamorphosis.     There  is,  however,  a  possibility  that 


248  ABRASION,  EROSION,  AND  STAINS. 

a  molecular  change  may  occur  as  a  result  of  time,  environment,^or 
impact  of  mastication. 

The  dentine  and  cementum  contain  about  28  and  30  per  cent, 
of  organic  matter,  respectively,  and  stain  deeply  and  permanently 
with  great  readiness. 

Possessed  of  living  cells  they  also  undergo  changes  in  their  structure 
under  the  influence  of  various  stimuli,  their  substance  being  added 
to  or  reduced  according  to  circumstances.  They  are  also  acted  upon 
by  mechanical  and  chemical  agencies,  if  exposed  to  their  influence. 

ABRASION. 

Abrasion  is  the  mechanical  wearing  away  of  tooth  substance. 

Occurrence.  It  occurs  most  commonly  upon  the  occlusal  surfaces 
of  teeth,  but  is  also  found  upon  the  proximal  surfaces,  the  labial  cervix, 
and  more  rarely  upon  the  lingual  cervix  alone.  It  is  also  seen  in  the 
temporary  denture,  especially  in  the  molars. 

Appearance.  Purely  abraded  surfaces  present  a  smooth,  flat,  or 
concaved,  highly  polished  appearance.  The  surface  may  become 
stained  or  otherwise  altered  in  color,  or  subsequent  caries  may  remove 
its  smooth  surface. 

Occlusal  Abrasion.  Occlusal  wear  is  very  common  and  occurs 
largely  with  men  who  chew  tobacco ;  the  contained  silex,  being  gritty, 
acts  as  an  abrasive.  Such  wear,  due  to  the  use  of  hard  food  or  gritty 
substances,  is  seen  in  skulls  of  aboriginal  man.  Some  degree  of 
occlusal  wear  is  accepted  as  normal  to  all  teeth,  the  act  of  mastication 
producing  marks  or  facets  at  the  point  of  articulation  of  antagonizing 
teeth.  A  tip-to-tip  variety  of  occlusion  permits  free  lateral  movement 
of  the  lower  jaw  and  an  herbivorous  type  of  articulation  causing 
abrasion.  It  is  also  frequent  in  those  cases  presenting  the  first  degree 
of  prognathism.  In  some  of  these  cases  the  labial  surfaces  of  the 
upper  incisors  and  cuspids  and  the  linguo-incisal  margins  of  the 
lower  incisors  are  worn.  A  single  overlapped  lower  tooth  may  abrade 
an  upper  tooth  in  this  manner. 

The  gritting  of  teeth  during  sleep  is  also  a  cause. 

The  undue  loss  of  posterior  occlusion  and  consequent  overuse  of 
the  anterior  teeth  cause  their  abrasion  after  the  manner  shown  in 
Figs.  261  and  274. 

Where  the  abrasion  occurs  in  a  fairly  regular  manner  four  degrees 
of  abrasion  are  classified  (Figs.  255  and  256):  (1)  abrasion  removing 
the  cusps;    (2)  abrasion  removing  the  occlusal  third  of  the  crown; 


ABRASION.  249 

(3)  abrasion  removing  the  middle  third  of  the  crown;  (4)  abrasion 
extending  to  the  gum  hne  or  beyond  (Broca). 

When  there  is  a  marked  overbite  occlusion,  with   a  consequent 
lessening  of  the  lateral  movement  of  the  mandible,  the  teeth  do  not 

Fig.  255. 


The  first  and  second  degrees  of  abrasion.     Specimens  from  museum  of  Philadelphia 

Dental  College. 

Fig.  256. 


The  third  and  fourth  degrees  of  abrasion.     Secondary  dentine  plainly  visible. 
Specimens  from  museum  of  Philadelphia  Dental  College. 

acquire  flattened  contact  surfaces,  but  their  cusps  increase  in  sharpness 
and  pointedness.  This  at  times  becomes  exaggerated  and  produces 
an  interlocking  of  cusps  or  rather  worn  surfaces  which  have  very 
sharp  edges. 


250  ABRASION,  EROSION,  AND  STAINS. 

In  the  first  degree  of  abrasion  the  dentine  is  often  hollowed  out  in 
atlvance  of  the  enamel  of  the  cusps,  forming  concave  places  in  which 
berry  seeds  lodge  and  cause  annoyance.  These  spots  are  at  times 
hypersensitive. 

Labial  and  Proximal  Abrasions.  Some  forms  of  abrasion  have  been 
attributed  to  too  vigorous  use  of  tooth-brushes,  particularly  when 
gritty  powders  are  employed.  There  is  no  doubt  that  mechanical 
abrasion  about  the  necks  of  teeth  is  produced  in  this  manner,  the 
gum  line  receding  beyond  the  enamel  border,  exposing  the  cementum : 
but  a  careful  examination  will  reveal  the  cementum  and  next  the 
underlying  dentine  to  be  affected;  the  enamel  is  not  abraded.  These 
tooth-brush  abrasions  are  quite  characteristic  (Fig.  257).  In  well-kept 
dentures  the  gums  are  seen  to  have  receded  from  their  normal  line, 
but  exhibit  no  evidences  of  turgescence;  the  roots  of  the  teeth,  upper 
and  lower,  are  exposed  to  a  greater  or  less  extent  along  their  labial 
and  buccal,  but  not  along  their  lingual  aspects ;  and  they  are  excavated 
to  variable  depths,  upon  the  bicuspids  and  first  miolars 
more  than  upon  the  other  teeth,  as  here  the  greatest 
force  of  brushing  is  received.  The  depressions  have  a 
normal  dentine  color,  sometimes  deepened  in  the 
mouths  of  non-smokers,  and  which  in  smokers  may 
be  periodically  blackened  by  deposits  of  carbon.  If 
caries  supervene,  the  abraded  areas  lose  their  normal 
color,  and  may  be  readily  indented  by  sharp  instru- 
ments, which  they  resist  before  the  advent  of  caries.  The  bicuspids 
and  molars,  particularly,  may  be  grooved  in  such  manner  as  to  require 
restoration  by  fillings.  The  condition  may  closely  simulate  some  forms 
of  erosion. 

A  clasp  may  abrade  a  tooth,  and,  if  food  debris  be  retained  on  its 
inner  side,  caries  may  follow  in  the  abraded  area.  The  purely  abraded 
surface  will  be  polished.  Slight  proximal  abrasion  may  be  normal 
as  a  facet,  due  to  the  rubbing  of  one  tooth  upon  another  at  the  contact 
point.  A  marked  example  of  this  was  seen  in  the  lower  jaw  of  a 
skull  of  a  Maori. 

The  third  lower  molars  are  locked  beneath  the  distal  surface  of 
the  crowns  of  the  second  molars.  Some  form  of  bone  loss  occurred, 
producing  looseness  of  the  third  molars.  The  individual  motion  of 
the  teeth  produced  a  deep  abrasion  of  the  enamel  of  the  second 
molars  upon  the  distal  surface  and  an  occlusoproximal  abrasion  of 
the  third  molars. 


ABRASION.  251 

Extensive  proximal  abrasion  may  be  due  to  extrusive  elongation 
of  a  tooth  in  one  or  both  jaws,  causing  a  tooth  to  occlude  with  its 
antagonist  with  a  glancing  motion. 

In  this  manner  specimens  are  produced  abraded  from  the  occluso- 
proximal  angle  to  nearly  the  apex  of  the  root. 

The  festoon  of  a  metal  plate  may  rapidly  cause  abrasion  of  the 
lingual  cervix  of  a  tooth.  The  condition  is,  however,  rare.  In  the 
editor's  practice  a  case  was  seen  in  which  several  teeth  were  so  affected 
in  a  few  months  by  an  ill-fitting  metal  plate.  The  festoon  of  a  vulcanite 
plate  has  also  produced  such  an  abrasion. 

Abrasion  sometimes  follows  caries  when  the  latter  has  become  freely 
exposed  to  attrition.  The  softened  surface  wears  away  and  the  part 
assumes  a  polished  appearance,  but  is  discolored  as  the  result  of  the 
stain  due  to  the  caries. 

It  is  probable  that  a  hyperacid  condition  of  the  saliva  in  connection 
with  mechanical  forces  may  be  a  cause  of  rapid  abrasion.  (See 
Erosion.) 

Effects  of  Abrasion.  These  are  external  and  internal,  and  most 
marked  in  the  occlusal  variety.  The  crown  wears  down  until  at  times 
the  gum  is  reached.  In  the  process  sharp  edges  of  enamel  are  formed. 
These  splinter  off,  leaving  rough  edges,  or  the  enamel  may  fracture 
or  split  longitudinally,  following  the  axis  of  the  crown.  Supported  by 
dentine  it  does  not  further  break  away  (Fig.  274). 

Sharp  enamel  edges  may  irritate  the  tongue,  producing  ulcers  of  a 
sometimes  chronic  type  which  acquire  indurated  edges  and  simulate 
syphilitic  sores  or  epithelioma.  The  causal  relationship  between  sharp 
edges  of  the  teeth  and  lingual  epithelioma  appears  to  be  quite  clear 
in  some  cases. 

Sores  which  have  given  evidence  of  malignancy  and  been  diagnosed 
as  malignant  growths  have  been  cured  by  rounding  and  polishing  sharp 
and  irritating  enamel  edges  of  teeth. 

The  continued  stimulation  of  the  ends  of  the  dentinal  fibrillse,  which 
are  exposed  in  abrasion,  causes  them  either  to  become  hypersensitive 
or  stimulates  them  to  formative  activity.  Tubule  material  is  built  upon 
the  inner  walls  of  the  tubule,  obliterating  their  lumen.  This  is  the 
so-called  tubular  consolidation  or  calcification  (eburnation).  Accom- 
panying this  secondary  dentine  is  often  formed.  As  a  result,  most 
commonly  the  pulp  chamber  of  the  crown  is  filled  up  with  secondary 
dentine  as  the  abrasion  proceeds,  and  the  crown  may  often  be  worn 
off  until  the  cervix  is  reached  while  the  pulp  remains  vital  and  covered 


252 


ABRASIOX,  EROSIOX,  AXD  STAINS. 


(Fiti.  256).  In  some  cases  the  abrasion  closely  approaches  the  pulp, 
which  for  some  reason  has  failed  to  protect  itself,  and  the  phenomena 
of  hypertiemia  or  even  exposure  and  its  results  occur. 

The  causes  and  phenomena  of  abrasion  of  the  temporary  teeth  are 
practically  the  same  as  in  the  case  of  adults,  except,  perhaps,  that 
children  are  more  subject  to  the  action  of  rectal  parasites,  as  ascaris 
lumbricoides,  taenia,  etc.,  or  suffer  from  irritable  bladder  due  to 
hyperacidity  of  the  urine.  These  conditions  commonly  produce  a 
reflex  stimulation  of  the  muscles  of  mastication,  resulting  in  nocturnal 
gritting  of  the  teeth. 

Treatment  of  Abrasion.  In  the  cases  of  cupped  occlusal  dentine, 
hard  fillings  of  gold  or  preferably  platinum  gold  are  advisable. 


Fig.  258. 


Fig.  259. 


Fig.  260. 


Gold  tip  for  abraded 
teeth  with  living  pulps. 
(Evans.) 


Gold  tip  for  abraded 
teeth  with  pulps  removed. 
(Evans.) 


Porcelain-faced  crowns 
for  teeth  with  living 
pulps.      (Evans.) 


If  nearly  all  teeth  are  present  and  the  abrasion  slight,  bridge-work 
may  be  used  to  restore  the  full  occlusion  without  attempt  at  restoration 
of  the  worn  surfaces. 

If  the  abrasion  of  the  upper  anterior  teeth  be  deep  the  bite  may 
be  raised  by  appropriate  posterior  crowns  or  bridges,  and  solid  platinum- 
gold  fillings  may  be  built  upon  the  anterior  teeth,  either  the  uppers 
alone  or  upon  both  the  upper  and  lower  teeth.  Anchorage  may  be 
obtained  in  the  dentine  or  screws  may  be  planted  in  the  dentine 
between  the  enamel  and  pulp  and  the  fillings  be  built  about  them. 
Instead  of  malleted  fillings,  tips  of  the  gold-inlay  type  may  be  made 
(Figs.  258  and  259). 

In  other  cases,  after  securing  a  proper  opening  of  the  bite  and 
posterior  occlusion,  single  porcelain-faced  gold  or  platinum  crowns 
may  be  made  to  cover  each  of  the  anterior  teeth.  For  this  purpose 
the  crown  is  appropriately  reduced  to  convenient  form,  but  the  pulps 


ABRASION.  263 

need  not  be  destroyed.  Fig.  260  represents  the  method  outhned  by 
Evans.^ 

Land  jacket  crowns,  consisting  of  a  wedge-shaped  platinum  jacket 
with  a  porcelain  facing  attached  by  means  of  one  of  the  numerous 
inlay  bodies,  may  be  used  instead  of  the  Evans  crown.  In  some  cases 
other  forms  of  crowns  may  be  indicated  (Fig.  262). 

There  present  at  times  cases  of  abrasion  in  which,  aside  from  the 
wear,  pyorrhetic  conditions  may  be  present,  or  where  bridges  cannot 
be  properly  inserted. 

If  this  pertain  to  the  upper  jaw  only,  the  lower  denture  may  be 
restored  to  usefulness,  the  upper  teeth  extracted,  and  a  full  upper 
denture  inserted ;  this  permits  the  adjustment  of  the  bite  to  any  desired 
level.  If  the  condition  be  transferred  to  the  lower  jaw  and  the  anterior 
teeth  be  in  good  condition,  a  piece  of  the  Griswold  type  may  be  fixed 
upon  cuspid  or  bicuspid  crowns. 

Fig.  261. 


Abrasion  of  anterior  teeth,  with  loss  of  posterior  occlusion.     (W.  A.  Capon.) 

It  is  to  be  remembered  that  in  any  case  of  opening  of  the  bite  the 
occlusion  is  to  be  restored  throughout. 

The  bite  must  not  be  raised  by  means  of  partial  plates  which  strike 
before  the  natural  or  crowned  teeth,  as  they  tend  to  embed  themselves 
in  the  soft  tissues  and  create  inflammation. 

If  the  bite  be  only  slightly  raised  by  plates  this  embedding  will 
cause  a  return  to  the  original  condition. 

In  case  of  hypersensitivity,  if  the  application  of  carbolic  acid, 
deliquesced  zinc  chloride,  Robinson's  remedy,  or  silver  nitrate  be  not 
effective,  nitric,  hydrochloric,  or  sulphuric  acid  must  be  applied  and 
the  resultant  softened  areas  later  filled. 

If  the  abrasion  be  caused  by  tobacco  its  use  should  be  stopped. 

A  difficult  class  of  cases  to  treat  is  found  in  those  highly  nervous 
individuals  who  grit  their  teeth  during  sleep.     It  is  probable  and 

1  Crown  and  Bridge  Worls;. 


254  ABRASIOX,  EROSION,  AXD  STAIXS. 

reasonable  that  this  cause  alone  may  serve  to  explain  abrasions  trace- 
able to  no  other  source.  The  cure  of  such  cases  as  these  could  only 
be  possible  through  the  wearing  at  night  of  some  modified  form  of 
interdental  splint.  The  cases  naturally  indicate  the  medicinal  use  of 
a  bromide  before  retiring,  unless  the  causes  can  be  discovered  and 
removed. 

If  such  gritting  be  present  in  children,  the  e^^dences  of  irritable 
bladder,  due  to  h^-peracidity  of  the  urine  or  of  rectal  parasites,  should 

Fig.  202. 


Same  case  as  Fig.  261.     Bite  opened  by  bridge-work,  posteriorly.     Anterior  teeth  restored 
by  means  of  Land  jacket  crowns.     (W.  A.  Capon.) 

be  sought  and  treated.  The  urine  may  be  rendered  alkaline  by  the 
use  of  potassium  salts  and  kept  so  by  restriction  to  a  largely  vegetable 
diet.  Belladonna  may  be  used  to  reduce  vesical  irritability.  Rectal 
parasites  may  be  removed  by  the  use  of  vermifuges  or  occasionally'^by 
rectal  injections. 

RESORPTION  OF  ENAMEL. 

Definition.  Resorption  of  enamel  is  the  removal  of  enamel  substance 
by  soft  tissue  containing  osteoclasts. 

Occurrence.  It  occurs  externally  only  in  impacted  teeth  surrounded, 
at  least  in  part,  by  irritated  tissue,  and  internally  very  rarely  after 
resorption  of  dentine  by  the  pulp.^ 

Pathology  and  Morbid  Anatomy.  Osteoclasts  approximate  the  enamel 
as  they  do  cementum,  decalcify  and  resorb  it.  The  dentine  is  next 
attacked.  There  result  irregular  excavations  (Howship's  lacunae)  and 
white  or  discolored  areas  of  evident  slight  decalcification  of  the  enamel. 
A  deposition  of  bone  into  the  area  may  occur.-  The  process  is  probably 
the  result  of  a  non-septic  inflammation  as  in  the  case  of  root  resorp- 
tion.    (See  Interstitial  Gingivitis.) 

1  Hopewell-Smith,  Histologj'  and  Pathohistology  of  the  Teeth.  2  ibij. 


EROSION. 


255 


The  enamel  may  be  resorbed  from  its  internal  surface  after  the 
resorption  of  dentine  by  the  pulp  (see  Chapter  XVIII.),  and,  as  shown 
by  Woods,^  may  be  filled  in  with  adventitious  material  of  a  structure 
resembling  cementum. 

Treatment.  Should  the  disease  by  chance  occur  upon  a  tooth  which 
later  has  been  drawn  into  place  the  area  may  be  filled,  otherwise  it 
has  only  a  pathological  interest. 

EROSION. 

Definition.  Erosion  of  the  teeth  is  a  term  applied  to  the  chemical 
or  chemicomechanical  destruction  of  the  hard  tissues  of  the  teeth 
in  such  a  manner  that  broad,  shallow,  smooth  excavations  are  made 


Fig.  263. 


Fig.  264. 


(Darby, 


CDarby.) 


Fig.  265. 


A  case  of  erosion  (drawn  from  the  cast) :  B,  silhouette  from  a  perpendicular  hne  through  the  left 
centrals,  upper  and  lower,  showing  the  loss  of  substance.     (Black.) 

in  the  enamel  and  dentine,  and  in  situations  in  which  dental  caries 
and  abrasion  are  least  likely  to  occur. 

The  excavations  occur  upon  surfaces  where  fermentative  processes 
occur  in  least  degree  and  where  there  is  no  marked  attrition.  Figs. 
263,  264,  and  265  illustrate  the  characteristic  appearance  of  areas  of 
erosion. 

1  Hopewell-Smith. 


256  ABRASION,  EROSION,  AND  STAINS. 

The  liibial  faces  of  the  anterior  teeth  are  more  frequently  affected 
than  tliose  of  any  of  the  other  teeth.  These  surfaces  appear  as  though 
sections  had  been  bodily  cut  out  of  them. 

The  enamel  is  affected  to  a  greater  extent  than  the  dentine,  forming 
shallow  excavations  in  the  teeth.  When  the  destructive  action  lays 
bare  the  dentine,  neither  it  nor  the  enamel  presents  any  of  the  appear- 
ances of  dental  caries,  the  eroded  surfaces  being  smooth  and  polished 
and  of  almost  normal  hardness. 

The  incisal  edges  of  the  anterior  teeth  are  sometimes  affected,  being 
cupped  out  in  a  manner  simulating  abrasion,  but  it  occurs  at  times 
in  teeth  which  are  distinctly  not  in  occlusion. 

Causes.  Dental  caries  always  presents  in  situ  softened  or  decalcified 
dentine.    Eroded  areas  sometimes  later  decay  in  part  when  the  nature 

of  the  effects  are  seen  to  be  dis- 
FiG.  266.  tinct.     The  only  other  condition 

with  which  it  may  be  confounded 
is  abrasion. 

As  individuals  are  seen  with  ero- 
sion who  have  never  used  a  tooth- 
brush (Fig.  266),  and  it  has  been 
seen  in  animals/  it  is  evidently  not 
caused  by  brushing,  yet,  as  will  be 
^    .      , ,  seen,    some    mechanical    element 

Erosion  of  lower  teeth  in  absence  of  use  of 

tooth-brush.    (Ivy.)  may  enter  as  a  factor. 

The  abrasion  of  mastication  evi- 
dently cannot  cause  it;  even  cases  of  marked  occlusal  abrasion  may 
not  be  accompanied  by  erosion. 

The  field  of  inquiry  is  therefore  narrowed  to  the  lip.  Lip  friction 
alone  is  incompetent,  as  it  occurs  in  every  mouth,  while  erosion  is 
comparatively  rare. 

As  only  acid  substances  can  dissolve  the  dental  tissues  in  the  mouth, 
the  inquirer  is  driven  to  the  conclusion  first  suggested  by  Truman 
that  erosion  is  due  to  an  altered  secretion  of  the  mucus-forming  glands 
of  the  lip  which  lie  in  close  relation  to  them.  Truman  found  these 
to  secrete  an  acid  at  night,  while  during  the  day  the  secretion  might 
be  alkaline.  The  disease  appears  to  affect  females  more  than  males, 
appears  usually  after  thirty  years  of  age,  and  usually  some  history  of 
gout,  rheumatoid  arthritis,  or  rheumatism  can  be  obtained.  Even 
when  the  existence  of  rheumatoid  or  gouty  affections  is  denied  by 

1   Tomes,  Dental  Surgery. 


EROSION.  257 

both  patient  and  medical  attendant,  it  is  rare  that  the  patient  does  not 
complain  of  some  general  disorder,  the  usual  ones  being  neuralgia  of 
long  standing,  marked  anaemia,  or  perhaps  neurasthenia.  Be  the 
condition  what  it  may,  the  essential  disease  process  is  one  which  may 
be  traced  to  the  effects  of  suboxidation  in  the  tissues. 

"If  the  orbicularis  oris  muscles  be  dissected  from  the  mucous  mem- 
brane of  the  lip,  the  labial  glands  may  be  observed;  they  are  more 
numerous  near  the  centre  than  at  the  extremities  of  the  lip"^ — i.  e., 
the  greater  number  overlie  the  labial  faces  of  the  incisors  toward  the 
necks  of  these  teeth.  "These  are  small,  racemose  glands,  their  ducts 
lined  with  low  granular  epithelium;  in  the  alveoli  the  cells  are  larger 
and  columnar  and  stain  less  readily  with  carmine."  "Their  secretion 
is  composed  of  water,  mucin,  and  inorganic  salts,  sodium  phosphate 
predominating,  which  gives  the  fluid  its  alkalinity  under  normal  con- 
ditions. In  conditions  of  irritation  and  consequent  hyperemia  the 
secretion  becomes  increased  in  amount  and  acid  in  reaction  (Kirk). 
The  nature  of  the  acid  is  not  clearly  known. 

Brubaker  has  suggested  the  theory  that  the  waste  products  of 
faulty  metabolism,  occurring  in  gout  and  kindred  conditions,  floating 
through  the  capillaries  of  the  labial  glands,  produce  irritation  and 
the  production  of  an  excess  of  carbon  dioxide.  This  exists  in  the 
cells  of  the  gland  as  carbonic  acid  H^Cog,  and,  combining  with  the 
alkaline  salt  sodium  phosphate  derived  from  the  blood,  the  following 
reaction  occurs:^ 

Alkaline  sodium       Carbonic  Acid  sodium  Sodium 

phosphate.  acid.  phosphate.  bicarbonate. 

HNa^PO,  +  H2CO3  =  H^NaPO,  +  HNaCog. 

The  acid  sodium  phosphate  formed  attacks  the  phosphate  and 
carbonates  of  calcium  composing  the  teeth  in  a  double  reaction  after 
the  manner  shown  in  the  following  equations: 

Calcium  Acid  sodium        Sodium  calcium       Acid  calcium 

phosphate.  phosphate.  phosphate.  phosphate. 

Ca3(PO;),  +  H^NaPO,  =  NaCaPO,  +  2HCaPO,. 

The  acid  calcium  phosphate  is  further  acted  upon  by  additional 
molecules  of  the  acid  sodium  phosphate  (dihydrogen  sodium  phos- 
phate) as  follows: 

Acid  calcium  Acid  sodium        Sodium  calcium  Diacid  calcic 

phosphate.  phosphate.  phosphate.  phosphate. 

2HCaP04  +  HaNaPO,  =  NaCaPO,  +  CaCH^POJa- 

1  Brubaker,  International  Dental  Journal,  December,  1894.  2  Ibid, 

17 


258 


ABRASION,  EROSION,  AND  STAINS. 


The  diacicl  calcic  phosphate  is  freely  soluble  and  doubtless  washed 
away  (Brubaker). 

The  reaction  upon  the  tooth  substance  is  but  incompletely  expressed, 
no  disposition  being  made  of  the  sodium  calcium  phosphate.  It  would 
seem  that  the  reaction  might  well  cease  with  the  production  of  the 
sodium  calcium  phosphate  and  acid  calcium  phosphate. 

Brubaker  immersed  a  tooth  for  a  week  in  a  solution  of  acid  sodium 
phosphate,  subjecting  it  daily  to  toothbrush  friction,  and  at  the  end 
of  that  time  spots  and  grooves  resembling  erosion  made  their  appear- 
ance.^ 

Fir..   2fi7. 


r?^ 


KCrr. 


3^.C 


ijK^ 


' 


Crystallization  of  salts  from  dialysate  of  saliva  from  erosion  case,  showing  two  typal  forms. 
Large  crystal  is  calcium  lactate.     (Kirk.) 


In  an  article  published  in  1902,  Kirk-  describes  polariscopic  experi- 
ments made  upon  saliva  from  a  patient  afflicted  with  a  general  erosive 
wasting  of  the  teeth.  The  saliva  of  the  patient,  who  was  a  sufferer 
from  inflammatory  rheumatism  and  its  associated  migraine,  etc.,  was 
dialyzed  and  the  dialysate  concentrated  and  found  to  contain  lactic 
acid  salts  (calcium  lactophosphate,  calcium  lactate,  and  magnesium 
lactophosphate).  Kirk  concluded  that  the  case  was  one  of  erosion 
due  to  lactic  acid  (Fig.  267). 

Kirk's  study  of  the  localized  cases  have  convinced  him  that  they 


1  It  is  to  be  understood  that   Brubaker  advances  this  explanation  hypothetically,  not  as  an 
assured  demonstration. 
"  Items  of  Interest. 


EROSION 


259 


are  produced  by  either  acid  sodium  phosphate  or  acid  calcium  phos- 
phate existing  in  an  abnormal  mucous  exudate  from  the  diseased 
labial  glands. 


Fig.  268. 


Another  field  from  the  ?aine  specimen  as  Fig.  267,  also  showing  two  typal  forms.     Large 
crystal  is  calcium  lactate.     (Kirk.) 

Fig.  269.  j. 


P^^H 

^^H 

^^^^^SJ^^I 

^^^^^H 

^^^^9 

^H|^^^^  ^3 

^^^^Ef^ '  'Hp'^^'^mI 

^EiJhH 

^^^■^^^H 

Crystallization  from  solution  of  a  tooth  in  1  per  cent,  lactic  acid.     Large  crystal  is  calcium 

lactate.     (Kirk.) 


Regarding  the  production  of  these  abnormal  exudates,  Kirk  argues 
that  in  diseases  of  suboxidation  the  blood  is  loaded  with  carbonic 


260  ABRASIOX,  EROSION,  AXD  STAIXS. 

acid  as  a  result  of  faulty  metabolism.  In  the  kidneys  the  mass  action 
of  the  carbonic  acid  upon  the  sodium  phosphate  of  the  blood  produces 
acid  sodium  phosphate  which  is  eliminated  in  the  urine,  and  sodium 
bicarbonate  which  is  returned  to  the  blood  and  maintains  its  alka- 
linity/ 

If  the  amount  of  carbonic  acid  produced  be  excessive  as  in  gout, 
the  labial  glands  also  take  up  the  action  and  produce  acid  sodium 
phosphate. 

It  is  to  be  noted  that  the  reaction  in  the  kidney  producing  acid 
sodium  phosphate  is  a  normal  one,  this  product  being  the  acid  salt 
of  the  urine  and  perspiration. 

It  is  also  to  be  remembered  that  in  gout  kidney  elimination  is  faulty, 
so  that  the  assumption  of  an  eliminative  function  by  the  labial  glands 
is  not  a  surprising  departure. 

It  is  a  point  of  importance  that  both  the  inorganic  and  organic 
matter  of  the  dentine  are  removed.  Experimentally,  a  10  per  cent, 
solution  of  acid  sodium  phosphate  will  do  this  rapidly.  Kirk"  stated 
that  he  was  only  once  able  to  produce  artificial  erosion  without  rough- 
ness by  the  simple  application  of  a  solution  of  acid  sodium  phosphate. 

Kirk  has  pointed  out  that  the  contents  of  the  labial  glands  in  cases 
of^rosion  gave  an  acid  reaction — /.  e.,  reddened  blue  litmus  paper — 
in  all  of  the  cases  tested  by  him. 

It  appears  to  be  almost  self-evident  that  there  must  be  some  modify- 
ing factor  causing  the  peculiar  forms  of  the  eroded  areas,  and  that 
it  must  be  an  abrasive.  In  many  of  the  cases  where  the  erosions 
are  in  the  form  of  transverse  grooves  there  is  no  doubt  that  the 
action  of  the  toothbrush  upon  the  decalcified  parts  removes  the 
latter;  the  areas  of  erosion  may  be  oval,  circular,  or  irregular  patches; 
again,  decalcification  may  appear  to  occur  over  the  entire  labial 
surfaces  of  teeth  uniformly;  however,  erosions  in  grooves  may  occur 
upon  the  teeth  of  persons  who  do  not  use  a  toothbrush  (Fig.  266). 
It  is  e\4dent  then  that  in  these  cases  the  mechanical  factor  must 
be  sought  in  the  muscular  movements  of  the  lips  and  tongue. 
The  greatest  effect  of  lip  movement  would  be  upon  the  entire  labial 
faces  of  the  central  incisors,  as  the  maximum  force  of  contact  of  lips 
with  teeth  is  at  and  near  the  median  line,  when  the  lips  are  alternately 
raised  and  depressed.  The  action  of  the  tongue  upon  the  labial  faces 
of  the  teeth  would  be  in  a  curved  line  passing  across  the  labial  and 

^  It  will  be  seen  that  this  is  a  modification  of  Brubaker's  theorj'. 
^  Private  communication. 


EROSION.  261 

buccal  surfaces  of  the  teeth,  beginning  at  the  occkisobuccal  portions 
of  the  first  molars,  and  having  its  highest  point  at  the  necks  of  tlie 
central  incisors. 

In  the  light  of  present  knowledge,  odd  and  isolated  situations  of 
areas  of  erosion  can  only  be  referred  to  localized  gland  affections,  the 
glands  overlying  the  spots  of  erosion  being  alone  affected. 

Black's  experiments  seem  to  show  that  the  production  of  a  current 
in  the  acid  fluid  used  as  a  test  medium  will  produce  the  erosive  effects. 

In  some  cases  existing  upon  the  sides  of  one  or  two  teeth  only,  it 
would  seem  that  there  must  exist  an  exudation  into  an  exact  area. 

Again,  certain  erosions  overhung  by  an  irritated  gum  margin  excite 
a  suspicion  that  the  gum  itself  may  cause  the  acid  exudate. 

Other  causes  for  erosion  have  been  cited. 

Guilford^  mentions  a  case  caused  by  shattuck  eating.  The  pitting 
of  grapes  with  the  teeth  has  produced  cases  of  peculiar  erosion  of  the 
labial  and  lingual  surfaces,  and  of  the  incisal  edges  of  anterior  teeth. 

Tomes^  instances  cases  of  erosion  caused  by  lemon  and  grape 
sucking. 

Morbid  Anatomy.  The  enamel  is  first  affected  as  a  minute  facet, 
which  deepens  until  a  transverse  groove  or  irregular  area  is  formed. 
The  cementum  is  often  involved,  and  when  reached  the  dentine  is 
cupped  out. 

The  erosion  form  shown  in  the  lower  jaw  of  Fig.  263  is  the  most 
common  and,  as  a  rule,  slowest  in  progress.  That  form  seen  on  the 
upper  cuspids  (Fig.  264)  is  also  quite  common. 

At  times  the  enamel  is  very  irregularly  removed,  and  at  times  sharp 
undercuts  are  formed.  In  other  cases  the  acid  action  seems  to  have 
been  distributed  over  the  whole  labial  face  (Fig.  265). 

Ivy  reports  a  case  of  erosion  in  a  patient  who  had  not  used  a 
toothbrush  for  fifteen  years.  The  erosion  was  confined  to  the  lower 
teeth  (Fig.  266). 

The  other  forms — ^labial  and  proximal  grooves — also  are  seen. 

The  surfaces  are  highly  polished,  and  the  dentine  hard,  but  has  a 
peculiar  horn-like  feel  to  cutting  instruments.  The  polish  is  retained 
after  calcining.^ 

The  dentine  also  often  becomes  more  translucent,  owing  to  tubular 
calcification.  Much  secondary  dentine  is  often  formed,  filling  the 
entire  coronal  pulp  chamber.  The  erosion  may  proceed,  exposing  this 
secondary  dentine,  and  when  the  groove  form  exists  the  grooving  may 

1  Lectures.  -  Dental  Surgery.  ^  Miller. 


262 


ABRASION,  EROSION,  AND  STAINS. 


extend  through  it.  The  tooth  is  necessarily  weakened  and  the  crown 
may  break  off;  such  a  result  is,  however,  very  rare.  The  pulp  is  very 
seldom  exposed. 

Fig.  270. 


FO 


SD 


—EC 


Sagittal  action  of  human  incisor  prepared  by  Mr.  Hopewell-Smith's  process,  and  stained 
■with  hajmatoxylin :  E  C,  erosion  cavity,  on  surface  of  which  can  be  seen  Baume's  clefts ;  P, 
pulp  tissue  undergoing  degenerative  changes;  FO,  atrophic  odontoblasts;  SD,  secondary 
dentine.    X  45.     (Hopewell-Sinith.) 

The  editor  has  noted  at  times  a  peculiar  grooving  upon  the  dentine, 
consisting  of  a  series  of  very  fine  lines.     The  lines  are  nearly  parallel 


EROSION.  263 

and  very  close  together.  The  inference  is  that  these  are  due  to  friction 
from  the  brush,  yet  they  may  not  be.  Baume  has  pointed  out  the 
existence  of  clefts  in  the  deepest  portion  of  the  erosion  areas 
(Fig.  270). 

The  course  of  erosion  may  extend  over  a  period  of  many  years, 
and  periods  of  erosion  with  periods  of  cessation  intervening  have  been 
noted.    This  would  indicate  periods  of  general  malnutrition. 

Gold  fillings  placed  when  erosions  are  small  are  left  as  raised  islands 
by  the  wasting  of  the  tooth  substance  around  them. 

The  acid  stimulation  of  the  dentinal  fibrillee  may  cause  great  hyper- 
sensitivity; as  a  rule,  however,  this  is  not  marked.  • 

The  anterior  teeth  are  sometimes  shortened  so  that  their  occlusion 
is  lost.  Kirk's  case  was  of  this  order.  The  shortening  may  be  due 
to  a  solution  of  the  incisal  enamel  and  dentine  imparting  a  wedge 
shape  to  the  incisal  edge,  or  a  distinct  cupping  of  the  dentine  may 
ensue.  At  times  the  carious  process  becomes  implanted  upon  an 
eroded  area,  or  at  some  part  of  it,  usually  the  cervical  portion.  This 
indicates  a  temporary  cessation  of  the  erosion. 

Diagnosis.  The  presence  of  the  peculiar  excavations,  the  hyper- 
sensitivity of  dentine  if  any,  and  the  acid  character  of  the  mucus 
from  the  follicles,  as  shown  upon  test  with  litmus  paper  made  just 
after  rising,^  are  diagnostic  signs.  The  acid  reaction  is  not  marked 
during  the  day.  The  existence  of  erosion  has  become  a  valuable  diag- 
nostic sign  for  the  general  practitioner  in  his  search  for  the  nature  of 
masked  maladies  from  which  patients  frequently  suffer.  Obscure  gout 
has  been  pointed  out  through  dental  indications  alone,  where  the 
practitioner  had  before  been  batfled  in  his  diagnosis. 

Treatment.  The  treatment  of  erosion  divides  itself  under  two  heads : 
prophylactic  and  restorative;  the  prophylactic  is  again  divided  into 
local  and  general  treatment.  The  problem  of  eradicating  the  cause 
of  the  disorder  lies  in  a  correction  of  the  morbid  glandular  secretion. 
It  is  evident  that  if  the  irritation  and  altered  secretion  of  these  glands 
be  due  to  some  systemic  cause,  a  disease  of  suboxidation,  notably  an 
affection  of  the  gout  order,  a  cure  of  the  local  disturbance  involves  the 
cure  of  the  underlying  systemic  cause. 

The  effect  of  an  antigout  regimen  and  antigout  therapeusis  upon 
the  advance  of  the  erosion  has  not  been  sufficiently  tested  or  observed 
to  furnish  reliable  data  in  this  connection,  but  so  far  as  tests  have 
gone  such  treatment  appears  to  lessen  the  formation  of  acid  substances 

'  Truman. 


264  ABRASION,  EROSION,  AND  STAINS. 

by  the  labial  glands.  Brubaker  has  suggested  the  advisability  of 
destroying  these  glands  by  means  of  the  electrocautery,  as  a  radical 
cure  of  the  progress  of  erosion. 

Next  in  importance  to  the  prevention  of  acid  formation  is  its  neutral- 
ization. This  implies  the  application  of  alkalies  or  the  use  of  alkaline 
mouth-washes.  The  greatest  production  of  acid  occurring  during  the 
night,  applications  of  adhesive  masses  of  alkaline  substances  are  made 
to  the  teeth  at  night.  The  principal  of  these  is  prepared  chalk,  calcium 
carbonate;  it  is  rubbed  over  the  labial  faces  of  the  teeth  and  between 
them,  before  retiring.  It  remains  in  sufficient  amount  to  neutralize 
any  acid  substances  coming  in  contact  with  it. 

Excellent  results  as  to  the  checking  of  the  progress  of  the  decal- 
cification are  obtained  from  the  use  of  magnesium  hydrate  held  in 
suspension  in  water,  milk  of  magnesia.  Kirk  found  that  three  hours 
after  the  use  of  a  teaspoonful  of  the  milk  of  magnesia  the  saliva 
maintained  an  alkaline  reaction.  It  should  be  used  at  night  as  a 
wash,  after  cleansing  the  teeth,  the  residue  to  be  left  as  an  alkaline 
coating  upon  the  teeth.  The  chalk  and  milk  of  magnesia  may  be 
mixed  into  a  paste.  If  the  preparation  be  disagreeable  a  few  drops 
of  oil  of  gaultheria  or  of  rose  may  be  added.  If  the  patient  care  to 
take  sufficient  trouble,  it  is  an  excellent  practice  to  dry  the  labial 
faces  of  the  teeth  each  evening  and  paint  them  with  a  solution  of 
amber  in  chloroform. 

It  has  been  suggested  by  Ottolengui^  that  in  the  earlier  stages  an 
impression  and  plaster  model  of  the  teeth  be  made  for  comparison 
at  future  dates,  so  that  the  progress  of  the  erosion  may  be  noted. 

Restorative  Treatment.  If  the  eroded  areas  be  excavated  and 
filled  the  erosion  may  proceed  about  the  edges  of  the  fillings.  It  may, 
however,  take  some  time  for  the  erosion  to  become  as  deep  as  the 
original  area. 

If  metal  be  used  the  margins  must  be  extended  to  avoid  this  if 
possible.  ^Nletal  is  very  unsightly  in  the  locations  peculiar  to  erosion, 
so  that  porcelain  inlays  which  the  locations  favor  are  indicated.  In 
their  place  gutta-percha  or  oxyphosphate  fillings  may  be  used,  but 
must  be  constantly  kept  in  a  good  condition  of  surface  or  they  become 
unsightly. 

The  generally  distributed  erosions  are  only  amenable  to  the  prophy- 
lactic treatment  (except  by  crowning  when  teeth  are  largely  wasted 
away),  and  slight  erosions  are  best  treated  in  the  same  manner. 

1  Methods  of  Filling  Teeth. 


MECHANICAL  INJURY  OF  THE  TEETH.  265 

MECHANICAL  INJURY  OF  THE  TEETH. 

It  was  pointed  out  on  page  156  that  the  enamel  is  a  material  much 
more  brittle  and  inelastic  than  the  dentine,  and,  therefore,  less  capable 
of  resisting  a  parting  strain.  Under  ordinary  circumstances,  however, 
well-formed  enamel  distributed  over  sound  dentine  resists  all  the 
ordinary  forces  brought  to  bear  upon  it. 

Under  abnormal  conditions,  however,  enamel  appears  to  fracture 
readily  in  two  directions :  (1)  along  the  line  of  the  interprismatic  cement 
substance  between  the  prisms  themselves;  (2)  along  the  Hne  of  cement 
substance  between  the  globules.  The  possibility  of  reference  of  all 
cases  into  one  or  other  class  indicates  that  the  cement  substance  is 
naturally  a  tissue  relatively  weak. 

Dentine  may  apparently  fracture  in  any  plane. 

Causes.  The  teeth  may  be  mechanically  injured  by  (1)  the  action 
of  abrasion,  which  mechanically  wears  away  the  teeth;  (2)  by  the 
application  of  undue  force  during  mastication  or  by  the  improper 
use  of  cutting,  filling,  or  extracting  implements;  (3)  by  blows  of  some 
sort  delivered  either  directly  upon  the  teeth  or  through  forcible  closure 
of  the  jaws,  as  the  result  of  a  shock  or  blow  delivered  upon  the  rim 
of  the  jaw. 

Aside  from  blows  or  bites  of  sufficient  force  to  break  sound  teeth, 
it  is  rare  to  find  teeth  fractured  without  a  previously  acquired  weakness 
in  the  tooth  itself.     The  causes  of  weakness  are  several. 

During  the  course  of  abrasion  the  enamel  is  worn  to  a  sharp  edge 
which  is  readily  fractured.  Oblique  splintering  occurs  in  the  line 
of  cement  substance  between  the  globules.  The  enamel  edges  become 
ragged  and  further  fracture  is  imminent.  Thread  biting  produces  a 
similar  but  localized  condition  (Fig.  274). 

Caries  by  removing  the  natural  support  of  the  enamel  renders  this 
brittle  material  subject  to  fracture  in  ordinary  use.  The  removal  of 
dentine  from  both  the  mesal  and  distal  sides  of  a  crown  by  caries — 
e.  g.,Si  bicuspid — renders  the  buccal  or  lingual  section  liable  to  fracture 
as  the  result  of  a  strain  delivered  between  the  cusps  and  tending  to 
wedge  them  apart.  This  accident  is  liable  to  occur  in  proportion  to 
the  lessening  of  the  healthy  dentine  between  the  cavities  or  beneath 
the  occlusal  fissure.  An  upper  incisor  so  decayed  would  naturally 
have  its  labial  section  fractured    away,  particularly  its  incisal  half. 

The  exposure  of  the  dentine  of  a  devitalized  tooth  to  the  saliva 
seems  to  weaken  it. 


266  ABRASION,  EROSION,  AND  STAINS. 

While  these  principles  are  correct  it  is  surprising  to  what  extent 
enamel  undermined  by  caries  may  retain  its  integrity  if  properly 
supported  by  an  adhesive  oxyphosphate  of  zinc. 

The  packing  of  cohesive  gold  against  frail  enamel  walls  renders 
them  liable  to  direct  fracture,  or  if  packed  so  as  to  permit  leakage 
the  wall  is  further  weakened  by  lactic  acid  produced  upon  its  under 
surface.  Again,  the  improperly  prepared  cavity  margin  may  be 
comminuted. 

Gold  does  not  support  enamel  walls  so  w^ell  as  oxyphosphate.  If 
built  over  comparatively  frail  walls  in  such  a  manner  as  to  protect 
them  from  direct  impact  they  stand  fairly  well. 

Amalgam  by  its  attendant  leakage  permits  gradual  weakening  of 
frail  enamel  w'alls. 

Johnson^  explains  fracture  after  filling,  w^here  the  enamel  walls 
were  previously  undermined  but  not  fractured,  upon  the  theory  that 
pre^'ious  to  filling  the  pain  attendant  upon  mastication  brings  about 
a  temporary  disuse  of  the  diseased  tooth.  After  filling  comfort  ensues, 
the  patient  again  uses  the  tooth,  and  fracture  occurs. 

The  fractures  caused  by  blows  present  features  of  interest.  An 
actual  splitting  off  of  one  of  the  angular  portions  of  a  crown  may 
occur,  or  a  fracture  may  be  seen  resembling  one  sometimes  seen  in 
a  pane  of  glass  the  result  of  a  light  blow  from  a  stone. 

In  the  latter  case  the  cracks  radiate  from  a  central  crushed  spot, 
and  may  involve  only  the  enamel.  A  large  section  of  an  incisor  may 
be  fractured  away  and  include  the  labio-incisal  third  and  all  the 
lingual  section  of  the  crown  and  a  small,  obliquely  fractured  portion 
of  the  root. 

Biting  upon  hard  objects  has  caused  the  fracture  of  sound  bicuspids 
and  molars,  the  line  extending  mesodistally  between  the  cusps,  and 
in  an  upper  tooth  through  the  crown  and  between  the  roots.  Thus, 
a  molar  or  first  bicuspid  may  be  divided  into  two  sections,  each 
supported  by  a  root  or  roots. 

Fracture  and  repair  of  enamel  after  eruption  is  not,  so  far  as  I  am 
aware,  known.    Cases  of  fracture  and  repair  of  dentine  have  occurred. 

A  case  of  such  repair  by  adventitious  (secondary)  dentine  has  been 
recorded  by  Tomes,^  and  Fig.  273  illustrates  a  fracture  of  the  root 
well  below  the  gum  line.  The  root  is  girdled  by  the  line  of  fracture, 
but  the  dentine  has  been  repaired  and  the  attachment  is  firm. 

1  Principles  and  Practice  of  Filling  Teeth. 
-  A  System  of  Dental  Surgery. 


MECHANICAL  INJURY  OF  THE  TEETH. 


267 


Longitudinal  cracks  in  the  enamel  of  otherwise  fairly  sound  teeth 
occur,  the  line  running  from  the  labial  edge  of  the  gum  to  the  incisal 
edge  of  an  incisor  (Fig.  274),  or  from  the  fissure  of  a  bicuspid  along 
the  enamel  to  the  summit  of  a  cusp,  or  from  the  cer\-ical  margin  of 
a  proximal  cavity  to  the  gum  margin. 


Fig.  271. 


Fig.  272. 


Oblique  fracture. 


Fracture  invoh-ing  the  bifurcation  of  the  roots. 


These  lines  probably  indicate  that  force  has  been  applied  sufficient 
to  cause  a  parting  of  the  enamel  cap  without  loss  of  continuity  in  the 
more  elastic  dentine.  Dryness  from  mouth  breathing  may  be  a  possible 
cause  of  cracks,  and  the  contact  of  excessively  hot  or  cold  substances 
has  been  advanced  as  an  hypothesis.     In  some  cases  the  enamel 


Fig.  273. 


Fig.  274. 


Root  fracture  and  re- 
attachment by  adven- 
titious dentine.  From 
a  specimen. 


Abrasion  associated  with  fracture 
of  the  enamel. 


cracks  may  be  very  numerous.  These  cracks  take  up  stains,  and  at 
times  in  the  preparation  of  cavities  cause  annoyance  by  centring 
the  chisel  and  perpetuating  a  defect  necessitating  the  removal  of 
much  tooth  tissue  or  the  risking  of  future  caries. 

Treatment.   The  treatment  of  fractures  involves  considerations  purely 
operative,  and  depends  upon  the  nature  of  the  case.     Roughened, 


268  ABRASION,  EROSION,  AND  STAINS. 

abraded  enamel  margins  are  best  rounded  with  carborundum  stones 
or  coarse  sandpaper  disks,  and  should  be  polished.  Sometimes  a 
deep  serration  must  be  filled;  corners  are  to  be  neatly  rounded  or 
restored  to  contour  by  fillings  or  inlays,  or  at  times  the  entire  incisal 
edge  is  to  be  ground  away  and  the  tooth  drawn  down  and  retained 
until  firm. 

In  case  of  an  uncompleted  tooth  root,  and  the  pulp  not  quite 
exposed,  a  pure  gold  all-metal  crown  is  to  be  adapted  with  or  without 
grinding,  according  to  the  future  requirements,  and  the  root  completion 
awaited. 

If  necessary  the  capping  of  the  pulp  may  be  attempted  as  well  for 
the  same  purpose. 

After  root  formation  the  pulp  may  be  destroyed  if  desired.  If 
conservation  of  the  pulp  be  not  possible  the  pulp  may  be  prepared 
for  removal  by  pressure  anaesthesia  or  cocaine  injection  and  the  root 
filled.     (See  Root  FilUngs.) 

Fractures  involving  the  cementum  demand  either  the  removal  of 
the  loosened  piece  and  the  construction  of  a  special  crown  retaining 
a  portion  of  the  natural  crown  as  a  base,  or  the  removal  of  all  of  the 
natural  crown  and  the  mounting  of  a  substitute  upon  the  root,  or  the 
parts  may  be  banded,  or  in  case  of  molars  an  all-metal  crown  may 
be  mounted.  In  some  cases  screws  must  be  placed  in  the  roots  and 
the  parts  restored  with  amalgam.  If  the  loosened  portion  be  retained 
oxychloride  of  zinc  or  thin  oxyphosphate  is  to  be  introduced  into  the 
joint  after  appropriate  sterilization  and  before  the  gold  crown  is  set. 
Should  the  pulp  be  vital  at  the  time  of  fracture,  it  will  become 
inflamed  and  should  be  removed  by  the  pressure  method  if  possible. 
To  accomplish  this  the  parts  must  be  lashed  together  and  an  occlusal 
opening  made.  The  requirements  vary  and  must  have  due  consid- 
eration. 


CHAPTER    XI. 

STAINS  OF  THE  ENAMEL  AND  DENTINE. 

Certain  stains  are  found  upon  the  surface  of  the  enamel  and  some- 
times penetrating  its  substance.  The  calculus  sometimes  located  upon 
the  enamel  is  not  included  in  this  consideration,  though  the  calculus 
itself  sometimes  becomes  stained.  So  far  as  they  have  been  observed 
stains  may  be  divided  into  those  of  metallic  and  non-metallic  origin. 

METALLIC  STAINS. 

Metallic  stains  are  those  which  are  caused  by  the  direct  deposition 
of  minute  particles  of  metal,  inhaled  by  workers  in  the  metals,  in  the 
organic  collections  upon  the  surfaces  of  the  teeth  or  taken  into  the 
mouth  in  various  solutions  of  drugs. 

Copper.  Miller  found  that  "workers  in  copper,  brass,  or  bronze 
all  presented  a  green  stain  upon  the  upper  teeth,  showing  every  shade 
of  green  and  bluish-green  up  to  bluish-purple.  The  latter  color  pre- 
dominated in  rooms  where  phosphor-bronze  was  worked."  Attention 
is  called  to  the  fact  that  "trumpeters  very  often  show  a  discoloration  of 
the  teeth."  Similar  discolorations  are  sometimes  noted  in  proximity 
to  copper-amalgam  fillings.  The  presence  of  copper  was  demonstrated 
in  scrapings  from  some  of  the  stained  teeth,  imparting  a  characteristic 
green  color  to  a  Bunsen  flame. 

Iron.  "Workers  in  iron  presented  stains  of  a  brownish  color." 
As  pointed  out,  "the  green  salts  of  iron  under  the  conditions  found 
in  the  mouth  would  become  oxidized  and  brownish  in  color."  The 
administration  of  iron  salts,  medicinally,  is  believed  to  produce  black 
discolorations,  iron  sulphide  being  formed.  "Iron  deposits  are  usual 
in  the  border  line  between  carious  and  normal  dentine."  It  is  usually 
believed  that  the  brownish  spots  frequently  seen  in  connection  with 
incipient  or  arrested  caries  of  the  underlying  enamel  are  due  to  the 
formation  of  iron  salts. 

Manganese.  Manganese  was  found  in  the  dark-colored  deposits 
upon  the  teeth  of  herbivorous  animals,  but  as  yet  not  upon  those  of 
man.  The  investigator  states  "that  alkaline  saliva  may  be  necessary 
to  the  production  of  these  deposits." 


270  STAIXS  OF  THE  ENAMEL  AND  DENTINE. 

Manganese  stains  may  occur  from  the  use  of  potassium  perman- 
ganate, manganic  oxide  being  formed. 

Mercury.  In  cases  of  prolonged  mercurial  administration  the 
deposits  (black)  upon  the  teeth  may  give  the  reaction  for  mercury. 
"If  mercury  and  potassium  iodide  are  given  together,  the  green  iodide 
of  mercury  might  be  present  upon  the  teeth."  It  is  probable  in  these 
cases  that  another  discoloring  substance  may  form.  There  is  in 
mercurialism  more  or  less  gingivitis;  the  gums  are  swollen  and  spongy, 
bleeding  readily.  "jNIore  or  less  putrefactive  decomposition  of  the 
albuminous  matter  present  upon  the  teeth  occurs,  and  hydrogen 
sulphide  is  formed.  Reacting  upon  the  oxyhsemoglobin  of  the  blood, 
sulphomethfemoglobin  is  formed — greenish-red  in  concentrated, 
green  in  dilute  solutions."  Miller  ascribes  the  discoloration  found  in 
conditions  of  gingivitis  from  various  causes,  with  lack  of  hygienic  care, 
to  a  probable  reaction  between  hydrogen  sulphide  and  oxyhsemoglobin. 

Lead.  Hirt  (quoted  by  Miller)  found  in  cases  of  lead-poisoning 
discolorations  upon  the  teeth:  dark  brown  at  the  necks,  light  brown 
on  the  crowns,  with  sometimes  a  trace  of  yellowish-green.  Miller's 
tests  (limited  in  number)  showed  no  lead  reaction  from  the  dental 
deposits  in  lead-poisoning. 

Nickel.  Some  of  the  salts  of  nickel  are  green.  "Metallic  nickel 
attacked  by  fluids  of  the  mouth  and  mixtures  of  bread  and  saliva  pro- 
duce greenish  salts.  The  entire  root  of  a  tooth  containing  a  nickel 
retaining  screw  has  been  stained  a  uniform  apple-green. 

Silver.  The  dentine  of  pulpless  teeth  containing  amalgam  fillings 
is  sometimes  stained  black,  owing  to  the  formation  of  silver  sulphide. 

The  use  of  silver  nitrate  as  a  wash  may  cause  the  albuminate  of 
silver  to  precipitate  metallic  silver  upon  the  teeth.  If  a  cavity  be 
touched  with  silver  nitrate  and  an  amalgam  filling  be  introduced 
the  metallic  silver  will  be  instantly  formed  at  any  point  where  the 
silver  nitrate  and  amalgam  combine.  If  this  be  upon  the  enamel  the 
latter  will  receive  a  somewhat  lasting  black  stain. 

The  nitrate  of  silver  applied  to  dentine  causes  the  dentine  to  assume 
a  light  yellowish-green  tinge,  and  the  albuminate  of  silver  is  formed; 
later  metallic  silver  is  precipitated,  the  tissue  becoming  black. 

Gold.  Gold  stains  may  be  formed  during  the  bleaching  of  teeth 
containing  gold  fillings  by  the  chlorine  methods.  The  dentine  becomes 
first  pink,  then  violet  or  purple,  then  black.^ 

^  Kirk,  American  Text-book  of  Operative  Dentistry. 


NON-METALLIC  STAINS  271 


NON-METALLIC  STAINS. 


Green  Stain.  This  most  common  of  green  deposits  upon  enamel 
occurs  upon  both  the  temporary  and  the  permanent  teeth,  particularly 
of  young  persons.  The  deposits  usually  have  a  crescentic  form,  are 
mainly  upon  the  labial  faces  of  the  anterior  teeth,  and  may  be  but  a 
narrow  line  or  may  cover  one-half  the  labial  face.  It  is  unusual  for 
the  deposit  to  extend  far  into  the  interproximal  spaces,  their  tendency 
being  to  follow  the  edges  of  the  proximal  surfaces.  While  green  stain 
undoubtedly  does  form  upon  adult  teeth  (Figs.  275  and  276)  where 
clearly  the  enamel  cuticle  has  long  been  absent,  it  is  only  very 
common  upon  young  teeth  where  remnants  of  Nasmyth's  membrane 
persist  about  their  necks.  The  color  of  these  deposits  varies  from 
light  green  to  greenish-black. 

Fig.  275.  Fig.  276. 


Extension  of  green  stain  on  the  approximal  Extension  of  green  stain  on  the  lingual 

surface  of  the  incisors.     (Miller.)  surface  of  incisors.     (Miller.) 

If  an  instrument  be  passed  over  the  portion  of  enamel  affected, 
more  or  less  roughness  of  the  surface  is  evident.  If  the  deposits  are 
subjected  to  friction  with  abrasives,  they  disappear  slowly  and  the 
enamel  beneath  may  be  found  roughened.  This  has  led  to  the  belief 
that  these  deposits  cause  decalcification  of  the  enamel.  It  is  found  upon 
adult  teeth  that  when  an  area  of  cervicolabial  enamel  has  become 
roughened  through  slight  decalcification  a  green  stain  is  likely  to 
form  upon  the  rough  surface  if  proper  hygienic  care  be  not  exercised. 
It  is  also  found  that  if  the  stain  be  removed  by  means  of  abrasives, 
the  roughened  enamel  may  be  readily  polished — i.  e.,  the  decalcification 
is  very  superficial. 

If  cases  be  observed  early  enough  in  childhood,  it  will  be  noted  that 
green  stain  is  usually  preceded  by  a  lack  of  oral  hygiene;  collections 
of  food  debris  are  not  removed  from  about  the  necks  of  the  teeth, 
which  implies  that  prior  to  the  formation  of  green  stain  the  affected 


272  STAIXS  OF  THE  ENAMEL  AND  DENTINE. 

enamel  surfaces  have  been  subjected  to  the  action  of  fermenting  food 
debris — that  is,  to  acids.  These  facts  have  led  to  an  acceptance  of 
the  view  that  the  roughness  or  decalcification  has  preceded  the  green 
deposits.  "If  teeth  be  placed  in  a  10  per  cent,  solution  of  hydrochloric 
acid,  in  from  two  to  four  minutes  the  enamel  cuticle  begins  to  loosen, 
and  in  from  five  to  ten  minutes  is  isolated.  It  is  found  that  the  entire 
stain  comes  away  with  the  cuticle." 

Nature  of  the  Coloring  Matter.  The  coloring  matter  is  found  to 
be  insoluble  in  water,  glycerin,  alcohol,  ether,  chloroform,  and  oil  of 
turpentine.  Mineral  acids,  hydrochloric,  nitric,  and  nitrohydrochloric, 
act  but  slowly  upon  the  coloring  matter;  even  hydrochloric  acid 
requires  some  hours  to  completely  destroy  it.  Tincture  of  iodine, 
commonly  believed  to  act  as  a  solvent  of  green  stain,  was  found  to 
affect  it  but  slightly.  Both  chlorine  and  nascent  oxygen  destroy  the 
coloring  matter  rapidly,  the  cuticle  being  bleached  in  a  few  minutes 
by  a  10  per  cent,  solution  of  hydrogen  dioxide.  Thick,  dark-green 
deposits  were  incompletely  bleached  after  eight  hours'  immersion  in 
the  10  per  cent.  HgO,  solution,  pointing  to  a  lack  of  uniformity  in  the 
composition  of  the  stain. 

The  belief  that  the  green  coloring  matter  is  chlorophyll  is  contra- 
dicted by  the  fact  that  it  is  not  soluble  in  ether. 

INIiller^  regarded  the  association  of  the  green  discoloration  with 
sulphomethaemoglobin,  or  some  allied  substance,  as  the  most  probable 
explanation,  though  he  found  a  micrococcus  in  a  deposit  of  green 
stain  which  produced  a  grayish-green  color  in  glycerin  agar, 

^Miller  did  not  find  any  definite  connection  between  a  milk  diet 
and  green  stain. 

Goadby^  has  found  B.  liquefaciens  fluorescens  motilis  present  in 
several  cases  of  green  stain.  It  deposits  in  its  culture  medium  a 
fluorescent  blue-green  pigment.  Other  mouth  bacteria  produce  a 
greenish  pigment — e.  g.,  B.  pyocyaneus  and  B.  fluorescens  non-lique- 
faciens.^  The  deposits  of  green  stain  are  considered  to  be  secondary 
to  enamel  decalcification  rather  than  the  cause  of  it,  when  found  in 
connection  with  it. 

In  case  of  roughened  enamel,  green  stain  appears  at  times  to  have 
been  taken  into  its  substance,  rendering  removal  without  bleaching 
difficult. 

Black  Stain.  A  peculiar  black  stain  occurs  in  the  mouth  of  appar- 
ently healthy  individuals,  both  men  and  women,  and  smokers  and 

1  Dental  Cosmos,  1894.  2  Mycology  of  the  Mouth.  3  ibid. 


DENTINE  STAINS.  273 

non-smokers,  and  even  with  those  who  also  neither  drink  tea  nor 
coffee.  It  occupies  the  general  position  described  for  green  stain,  but 
may  cover  much  of  the  surface  of  the  teeth.  It  occurs  in  somewhat 
unclean  mouths,  though  the  teeth  may  have  been  regularly  brushed. 
As  a  rule  those  teeth  having  the  deposit  are  comparatively  free  from 
caries.  Its  etiology  is  not  worked  out,  but  it  may  be  due  to  a  forma- 
tion of  iron  sulphide  in  place  of  sulphometha^moglobin.  It  is  very 
readily  removed  and  does  not,  as  a  rule,  affect  the  enamel.  At  times 
a  superficial  caries  is  found  associated  with  it,  and  at  some  minute 
spot  the  enamel  may  be  penetrated.  Whether  this  cavity  is  a  result 
of  the  action  of  the  film  is  not  certain. 

Tobacco  Stains.  Smokers  have  characteristic  black  deposits  upon 
both  the  teeth  and  calculus  deposited  upon  them.  The  stain  is  most 
marked  upon  the  lingual  surfaces  of  the  teeth,  and  a  pipestem  held 
well  back  in  the  mouth  may  cause  a  thick  deposit  upon  some  of 
the  posterior  teeth. 

Tobacco  juice  itself  stains  exposed  dentine  and  cementum,  and 
enters  cracks  in  the  enamel,  producing  brown  discolorations  very 
difficult  or  impossible  to  remove. 

Red  Stain.  A  peculiar  red  stain  occurs  upon  the  necks  of  some 
teeth,  but  is  not  generally  distributed.  It  is  probably  due  to  chromo- 
genic  bacteria,  as  it  is  only  found  in  unclean  surfaces. 

According  to  Goadby,^  B.  prodigiosus,  B.  rouge  de  Kiel,  B.  mesen- 
tericus  ruber,  B.  roseus,  sarcina  roseus,  micrococcus  roseus,  and 
other  micrococci  produce  a  red  pigment  in  at  least  some  of  their 
media. 

Sarcina  lutea  and  sarcina  aurantiaca  produce  yellow  and  orange- 
colored  pigment,  respectively.^  The  exact  relation  of  chromogenic 
bacteria  to  stains  is  not  worked  out. 

DENTINE  STAINS. 

Exposed  dentine  may  be  stained  as  enamel  is.  In  addition  it  may 
take  up  certain  stains  like  tobacco. 

Metallic  fillings,  such  as  amalgam,  containing  mercury,  silver, 
copper,  or  cadmium  metals  which  combine  with  sulphuretted  hydrogen 
to  form  sulphides,  may  cause  staining  of  dentine. 

Metallic  posts  containing  silver,  copper,  or  nickel,  or  made  of  steel 
or  iron  wire,  may  produce  sulphides  in  the  same  manner.    The  dentine 

1  Mycology  of  the  Mouth.  ^  Ibid. 

18 


274  STAINS  OF  THE  ENAMEL  AND  DENTINE. 

may  also  be  stained  pink  by  haemoglobin  entering  the  tubules  during 
the  progress  of  venous  hypersemia. 

The  dentine  may  also  be  stained  by  iron  sulphide,  formed  during 
putrefaction  of  the  pulp,  by  the  action  of  hydrogen  sulphide  upon  the 
iron  contained  in  the  hremoglobin  of  the  blood  undergoing  decom- 
position. 

TREATMENT  OF  STAINS. 

Enamel  stains  are  best  removed  by  mechanical  means,  after  the 
removal  of  calculus  from  the  teeth.  (See  Salivary  Calculus.)  For  this 
purpose  brush  wheels  and  rubber  cups  charged  with  pumice  and 
revolved  in  the  dental  engine  are  used  to  remove  the  accessible  portions 
of  the  stains.  Next  a  wood  point,  made  by  sharpening  an  orange- 
wood  stick  to  a  wedge-shape,  is  charged  with  the  pumice  and  rubbed 
by  hand  over  all  the  surfaces  not  reached  by  the  brushes  and  cups. 
For  the  more  inaccessible  situations  the  point  is  to  be  mounted  in  a 
Cogswell  or  other  carrier.  A  very  fine  linen  tape,  a  German-silver 
strip,  or  floss  silk  charged  with  the  pumice  will  remove  the  stains  at 
the  contact  points. 

The  powdered  pumice  used  is  best  mixed  with  glycerin  to  prevent 
the  flying  of  the  pumice  during  the  rapid  revolution  of  the  wheels. 
Saturation  of  the  stains  with  tincture  of  iodine  renders  them  more  visi- 
ble and  also  brings  to  view  the  associated  bacterial  films  upon  the  teeth. 

Register  recommends  the  use  of  1  per  cent,  hydrogen  dioxide  to 
be  forcibly  sprayed  upon  the  gums  and  deposits  both  before  and  after 
the  use  of  tincture  of  iodine.  The  brush  and  pumice  will  then  rapidly 
remove  the  stains  and  bacterial  films  upon  the  accessible  portions 
of  the  teeth. 

Tobacco  stains  in  cementum  need  not  be  removed  to  their  full  depth. 

Head^  has  suggested  the  removal  of  deep  enamel  stains  and  the 
deposits  in  irregular  depressions,  inaccessible  to  the  stick,  by  the 
use  of  nascent  oxygen  derived  from  25  per  cent,  ethereal  pyrozone 
or  a  paste  of  sodium  dioxide  and  water,  made  by  dissolving  the  latter 
in  distilled  water  at  about  32°  F.  These  are  applied  to  the  part  on 
cotton,  and  nascent  oxj^gen  liberated  with  a  hot  burnisher.  The  face 
and  gums  are  protected  by  the  securely  placed  rubber-dam  and  by 
oiling  the  face. 

The  method  is  also  apphcable  to  the  bleaching  of  obstinate  stains 
of  the  dentine,  especially  near  the  cutting  edges. 

'   Items  of  Interest,  1902. 


TREATMENT  OF  STAINS.  275 

If  beneath  green  stains  decalcification  be  discovered,  the  decalcified 
area  should  be  removed,  the  enamel  polished,  and  the  patient  urged 
to  careful  prophylaxis. 

After  the  removal  of  calculus  and  stains  from  the  teeth  the  mouth 
and  teeth  should  be  kept  in  as  cleanly  and  aseptic  a  state  as  possible 
by  the  employment  of  correct  prophylactic  measures.  Dental  caries 
and  pyorrhoea  alveolaris  are  thus  also  largely  prevented.  (See  Prophy- 
laxis of  Dental  Caries  and  Pyorrhoea  Alveolaris.) 

The  stains  found  in  the  dentine  are  also  divisible  into  metallic  and 
non-metallic.  The  former  are  best  removed  by  transforming  the 
insoluble  metallic  salt  into  a  soluble  one. 

The  most  frequent  and  practicable  course  is  to  form  soluble  chlorides 
through  the  action  of  nascent  chlorine.    Copper,  nickel,  gold  and  iron 
stains  should  be  subjected  to   the  chlorine  method   of    bleaching, 
followed  by  repeated  washings  with  chlorine  water,  50  per  cent.,  and. 
hot  distilled  water  to  remove  the  chloride  formed.^ 

Silver  stains  are  converted  into  silver  chloride  by  the  chlorine  method, 
or  iodide  by  the  use  of  tincture  of  iodine,  and  dissolved  out  by  the  use 
of  sodium  hyposulphite  followed  by  hot  distilled  water.^ 

For  mercurial  stains  Kirk  recommends  the  use  of  aqueous,  ammo- 
niacal  solution  of  hydrogen  dioxide  after  the  chlorine  method,  and  a 
saturated  solution  of  potassium  iodide  after  the  iodine  method,  in 
either  case  followed  by  washing  with  hot  distilled  water. 

Manganese  stain  is  removable  by  the  use  of  25  per  cent,  aqueous 
solution  of  hydrogen  dioxide  saturated  with  oxalic  acid  crystals  and 
followed  by  washing  with  hot  water. 

The  non-metallic  dentine  stains  are  removable  by  the  use  of  nascent 
chlorine  evolved  from  chlorinated  lime  by  the  reaction  with  dilute 
acetic  acid  or  of  nascent  oxygen  evolved  from  hydrogen  dioxide  or 
sodium  dioxide. 

In  either  case  the  color  molecule  is  destroyed  by  the  indirect  or 
direct  oxidizing  effect. 

The  hydrogen  dioxide  may  be  used  in  the  form  of  the  25  per  cent, 
ethereal  solution  (25  per  cent,  pyrozone)  applied  for  a  time  or  sealed 
within  the  tooth  for  twenty-four  hours,  or  the  25  per  cent,  aqueous 
solution  may  be  driven  into  the  tubuli  by  the  aid  of  the  cataphoric 
current. 

Sodium  dioxide  should  be  employed  in  saturated  solution  in  distilled 
water  (made  at  about  32°  F.).     The  dentine  is  first  desiccated  and 

1  Kirk.  2  Ibid. 


276  STAINS  OF  THE  ENAMEL  AND  DENTINE. 

then  saturated  with  the  solution.  Weak  sulphuric  acid  (10  per  cent.) 
is  used  to  liberate  the  nascent  oxygen.  Kirk  recommends  a  second 
application,  omitting  the  use  of  the  acid. 

As  with  metallic  stains,  all  the  by-products  should  be  washed  out 
with  hot  distilled  water.^ 

^  For  a  complete  description  of   the  bleaching  process,  see  Kirk'a  article  in  American  Text- 
book of  Operative  Dentistry. 


C  H  A  P  T  E  R    X  1 1. 

DENTAL    CAEIES:      HISTORY;     EXCITING    AND    PEEDISPOSING 

CAUSES. 

Definition.  Dental  caries  may  be  defined  as  a  disease  of  a  tooth 
characterized  chiefly  by  the  production  of  a  locaHzed  ca\aty,  concavity, 
or  area  containing  decalcified  tooth  structure  and  due  to  a  combined 
acid  fermentation  and  Hquef action. 

History.  Examinations  of  crania  show  the  disease  to  be  certainly 
as  old  as  semicivilization,  and  when  more  data  are  obtainable  it 
will,  no  doubt,  be  found  even  older.  The  skull  of  a  mummy  in  the 
British  Museum,  dating  2800  B.C.,  exhibits  well-marked  caries  and 
other  dental  diseases.  Caries  appears  in  the  teeth  of  the  skulls  of" 
all  peoples,  no  matter  what  their  degree  of  civilization,  provided^ 
their  dietary  included  cooked  starchy  foods.  i 

Causes.     These  may  be  divided  into  exciting  and  predisposing. 

Prior  to  the  investigations  of  Miller,^  published  in  1882,  a  vast 
amount  of  labor  was  expended  in  the  effort  to  determine  the  cause 
of  dental  caries.  The  deductions  made  were  partly  speculative  and 
partly  based  upon  scientific  investigations. 

From  1754  to  1835  caries  was  regarded  as  an  inflammation  or 
gangrene  of  tooth  structure;  Boudett,  Jourdain,  Hunter,  Fox,  Bell, 
Fitch,  and  Koecker  advancing  one  or  the  other  theory.^  ^ 

In  1835  Robertson,^  of  Birmingham,  England,  advanced  the  opinion, 
based  upon  his  observ^ations,  that  it  "is  to  chemical  and  not  to  inflam- 
matory action  that  the  destruction  of  the  teeth  must  be  attributed. '' 
The  author  points  out  forcibly  the  errors  and  fallacies  of  previous 
writers.  He  states  that  "Particles  of  food  retained  in  fissures  and 
imperfections  of  the  teeth  and  in  the  spaces  between  the  teeth  undergo 
a  process  of  decomposition  and  acquire  the  property  of  corroding, 
disuniting,  and  therefore  destroying  the  earthy  and  animal  substances 
of  which  the  teeth  are  composed." 

1  International  Dental  Journal,  1884. 

2  For  an  interesting  and  exhaustive  exposition  of  their  views,  see  American  System  of  Den- 
tistry, Section  on  Dental  Pathology,  by  Black. 

3  A  Practical  Treatise  on  the  Human  Teeth,  second  edition,  Philadelphia,  1839. 


278  DENTAL  CARIES. 

John  Tomes,  a  little  later,  was  the  first  to  record  microscopic  exam- 
inations of  carious  dentine.  He  described  the  transparent  zone  lying 
between  the  carious  and  non-carious  dentine,  and  observed  and 
pointed  out  also  the  dentinal  fibrilloe.  He  announced  the  very 
significant  fact  in  relation  to  caries,  that  if  blue  litmus  paper  be  applied 
to  a  carious  cavity  it  is  at  once  reddened,  which  furnishes  evidence 
of  the  presence  of  an  agent  capable,  if  unresisted  by  the  vitality  of 
the  dentine,  of  depriving  the  tissue  of  its  earthy  constituents,  leaving 
the  "gelatin  to  undergo  a  gradual  decomposition  favored  by  the  heat 
and  moisture  of  the  mouth." 

Tomes  first  established  the  essentially  chemical  character  of  some 
features  of  caries.  The  character  of  the  acid  and  its  localization  were, 
however,  not  ascertained. 

In  1S67  Bridgman  promulgated  the  theory  that  the  crown  of  the 
tooth  and  the  gum  were  of  different  electric  potential,  and  that  being 
bathed  in  the  oral  fluids  the  conditions  of  a  battery  were  set  up. 

Acid  substances  were  said  to  be  set  free  at  the  positive  pole  (the 
crown)  causing  decalcification. 

S.  B.  Palmer,  in  1874,  claimed  that  after  filling  recurrent  caries  was 
caused  by  the  conditions  of  a  battery  being  set  up — i.  e.,  the  difference 
of  electric  potential  between  the  filling  and  dentine  in  the  presence 
of  saliva  or  of  the  fluid  of  the  dentine  as  an  electrolyte  caused  liberation 
of  acids,  producing  decalcification  of  the  tooth  or  disintegration  of 
the  filling— e.  g.,  oxj'phosphate. 

Miller,  in  1S81  and  1900,^  experimentally  examined  these  assump- 
tions. He  ground  the  enamel  away  from  the  crowns  of  freshly  ex- 
tracted teeth  and  filled  cavities  made  in  them  with  gold  and  gutta- 
p^cha.  These  he  placed  in  separate  flasks  containing  a  physiological 
salt  solution  (0.75  per  cent,  table  salt).  This  in  the  presence  of  electric 
currents  should  produce  hydrochloric  acid  by  liberation  of  hydrogen 
and  chlorine,  and  decalcification  should  occur.  After  four  years 
there  was  no  decalcification. 

Similarly  filled  teeth  were  suspended  in  dilute  lactic  acid.  The 
decalcification  was  exactly  similar  to  that  in  the  unfilled  pieces  used 
as  a  control.  Had  electrolytic  currents  been  generated  between  the 
metals  and  dentine  the  latter  would  have  been  acted  upon  more  vigor- 
ously than  in  the  unfilled  pieces. 

In  1868  Watt^  advanced  the  theory  that  free  sulphuric,  nitric,  and 

1  Dental  Cosmos,  April  1901. 
-  Chemical  Essays,  1868. 


HISTORY  AND  EXCITING  CAUSES.  279 

hydrochloric  acids  were  generated  in  the  mouth  during  putrefaction 
processes  and  caused  the  different  varieties  of  caries. 

Magitot^  pointed  out  that  the  essential  phenomena  of  caries,  as  they 
were  then  understood,  were  the  same  in  natural  teeth  mounted  upon 
plates  as  in  the  natural  organs  iji  situ;  proving  that  caries  is  intrinsic- 
ally independent  of  the  existence  of  vitality.  By  immersing  teeth  in 
solutions  of  sugar  undergoing  fermentative  changes  he  found  that 
decalcification  occurred.  Teeth  immersed  in  solutions  of  sugar  in 
which  fermentation  had  been  prevented  by  boiling  the  solution  and 
sealing,  or  by  additions  of  sufficient  carbolic  acid,  remained  unaffected. 

Leber  and  Rottenstein,  in  1867,  first  called  attention  to  the  probable 
causative  association  of  bacteria  with  some  phases  of  dental  caries.  By 
staining  carious  dentine  with  iodine  the  dilated  dentinal  tubules  were 
shown  to  be  filled  with  granular  bodies,  which  they  recognized  as 
bacteria,  identifying  but  one  of  the  many  forms  of  oral  bacteria — the 
leptothrix.  They  deemed  an  initial  exposure  of  dentine  a  necessary 
preliminary  to  the  invasion  and  growth  of  the  leptothrix,  which  in 
conditions  of  lessened  resistance  gained  access  to  the  tubules  and  in 
some  undescribed  manner  caused  their  dilatation. 

The  question  of  the  recognition  of  the  presence  of  bacteria  directly 
resolves  itself  into  the  subject  of  special  staining.  Prior  to  the  work 
of  Koch,  presented  in  1881,  no  means  of  isolating  specific  bacteria  by 
special  cultures  and  staining  were  known,  and  it  is  remarkable  that  in 
the  same  year  the  essential  features  of  dental  caries  were  first  made 
out  with  some  degree  of  clearness. 

Miles  and  Underwood  (World's  Medical  Congress,  1881)  point  out 
clearly  and  at  length  the  different  appearances  produced  by  simple 
decalcification  of  dentine  and  those  by  dental  caries.  Speaking  of 
Magitot's  experiments,  they  say:  "We  assume  that  two  factors  have 
always  been  in  operation:  (1)  the  action  of  acids  and  (2)  the  action  of 
germs.  AVhen  caries  occurs  in  mouths  it  is  always  under  circumstances 
more  favorable  to  the  action  of  germs  than  to  the  action  of  acids." 
They  believed  that  the  acids  necessary  for  the  decalcification  were 
excreted  by  the  germs,  which  utilized  the  dentinal  fibrillse  as  a  food 
supply. 

It  will  be  seen  that  the  invasion  and  multiplication  of  organisms  in 
the  tubuli  were  held  as  the  antecedent  of  the  process  of  decalcification. 
The  deductions  of  these  gentlemen  were  drawn  from  data  not  derived 
from  the  methods  of  modern  bacteriology — i.  e.,  special  stains  and 

1  Treatise  on  Dental  Caries,  Experimental  and  Therapeutical  Investigations. 


280  DENTAL  CARIES 

special  cultures.  Moreover,  they  were  made  before  the  physiological 
chemistry  of  bacteria  was  even  partially  understood. 

In  1882  AV.  D.  Miller,  of  Berlin,  announced  as  the  results  of  experi- 
ments conducted  by  him  that  he  believed  the  first  stage  of  dental  caries 
to  consist  of  a  decalcification  of  the  tissues  of  the  teeth  by  acids  which 
are  for  the  greater  part  generated  in  the  mouth  by  fermentation.  This, 
it  will  be  seen,  is  a  position  in  agreement  with  that  of  Leber  and  Rotten- 
stein,  rather  than  with  that  of  INIiles  and  Underwood. 

Miller's  observations  and  experiments  established  the  following 
basal  facts  in  connection  with  dental  caries: 

1.  That  in  all  cases  of  dental  caries  micro-organisms  may  be  seen 
under  the  microscope  in  the  tubules  of  the  carious  dentine,  and  that 
bacteria  exist  in  great  numbers  in  the  mouth. 

2.  That  the  invasion  of  the  tubules  is  always  preceded  by  decalci- 
fication of  the  dentine— I.  e.,  an  area  sometimes  relatively  large  of 
decalcified  dentine  may  be  seen  in  advance  of  the.  organisms. 

3.  Analysis  of  the  softened  dentine  proved  that  a  large  part  of  its 
lime  salts  were  removed — /.  e.,  decalcification  had  occurred. 

4.  Test  with  litmus  paper  gave  the  acid  reaction  in  nearly  every 
case,  so  that  the  inference  that  decalcification  was  due  to  an  acid  was 
warrantable. 

5.  The  food  substances  taken  into  the  mouth  are  of  all  classes. 
Carbohydrates  (sugars  and  starches),  hydrocarbons  (fats),  and  nitrog- 
enous (albuminous)  materials. 

The  carbohydrates  are  fermented  with  acid  reaction  by  many  mouth 
bacteria,  commonly  producing  lactic  acid;  the  albumins  ferment  with 
an  alkaline  reaction. 

It  w^as  inferred  from  this  and  other  experiments  that  caries  was  due 
to  the  acid  fermentation  of  carbohydrates  and  not  directly  to  the 
fermentation  of  albuminous  substances. 

6.  That  oral  fermentation  is  the  result  of  bacterial  action  his  follow- 
ing fundamental  experiments  show: 

(a)  A  small  tube  was  filled  with  a  solution  of  starch  and  fastened 
to  a  molar  tooth  on  retiring.  The  next  morning  the  contents  of  the 
tube  had  a  strong  acid  reaction.  A  tube  of  the  starch  solution  with 
saliva  added  was  incubated  at  blood  temperature.  After  four  or  five 
hours  the  mixture  became  acid. 

(6)  The  mixture  of  starch  and  saliva  was  kept  at  100°  C.  for  a  half- 
hour  and  incubated.  It  did  not  become  acid — i.  e.,  the  exposure  to 
this  temperature  killed  the  ferment. 


HISTORY  AND  EXCITING  CAUSES.  281 

(c)  The  saliva  was  boiled  for  a  half-hour  and  then  added  to  the 
starch  solution  and  the  mixture  incubated.  No  acid  was  produced — 
i.  e.,  the  ferment  existed  in  the  saliva,  not  in  the  starch. 

(d)  The  ptyalin  of  the  saliva  was  destroyed  by  heating  the  mixture 
for  twenty  minutes  at  67°  C. ;  the  incubated  mixture  still  became  acid 
— i.  e.,  ptyalin  did  not  act  as  the  acid-forming  ferment,  but  the  fermen- 
tation must  have  been  caused  by  some  other  ferment  not  destroyed  by 
exposure  to  this  temperature. 

(e)  To  the  mixture  of  saliva  and  starch  carbolic  acid  was  added 
as  an  antiseptic.    No  acid  was  formed,  but  the  ptyalin  formed  sugar. 

(/)  A  number  of  tubes  were  each  supplied  with  a  small  quantity  of 
the  saliva-starch  solution  and  sterilized;  a  third  of  them  were  infected 
from  the  mouth,  a  third  by  carious  dentine,  and  a  third  were  left 
uninfected  as  controls.  The  infected  tubes  became  acid;  the  controls 
did  not. 

(g)  The  first  of  a  series  of  tubes  containing  sterilized  saliva  and 
starch  solution  was  infected  with  carious  dentine;  when  this  became 
acid  a  fraction  of  a  drop  was  carried  from  it  to  a  second  tube.  After 
that  became  acid  a  third  was  infected  from  it  and  so  on  indefinitely. 

Conclusion.  Carious  dentine  contains  a  ferment  or  ferments 
capable  of  reproduction — i.  e.,  living  organisms  are  present  in  it. 

7.  The  nature  of  this  living  ferment  was  determined  by  infecting 
a  culture  medium  with  carious  dentine  taken  from  the  deeper  layers. 
The  bacteria  cultivated  were  distended  into  pure  cultures  by  carrying 
through  a  series  of  cultures  and  examining  microscopically  during 
the  process.  The  same  morphological  characteristics  were  exhibited 
in  the  last  tube  as  shown  by  the  germs  in  the  deeper  layers  of  carious 
dentine  itself,  and  was  identical  with  that  of  bacterium  acidi  lactici. 
These  germs  may  be  found  in  the  sediment  of  a  culture  tube  and 
consist  of  cocci  and  micrococci,  either  single  or  in  chains.  These 
cocci  possess  the  power  of  forming  lactic  acid  from  glucose.  The 
organism  is  a  facultative  anaerobe  (Fig.  277). 

8.  A  sound  bicuspid  was  sawed  into  sections  and  an  equal  number 
of  these  sections  placed  in  each  of  two  test-tubes.  Upon  these  was 
poured  a  2  per  cent,  acjueous  extract  of  beef  (albuminous).  To  one 
tube  a  minute  portion  (0.2  per  cent.)  of  cane-sugar  was  added.  Both 
tubes  were  sterilized  and  after  cooling  infected  with  a  pure  culture 
of  the  germ  obtained  from  the  deeper  layer  of  carious  dentine.  The 
sugar-containing  solution  became  acid  in  a  few  hours;  in  a  week  the 
dentine  was  softened;  in  two  weeks  thin  sections  were  completely 


282  DENTAL  CARIES. 

decalcified;  in  three  weeks  cavities  were  found  in  the  dentine  exactly 
similar  to  cavities  formed  in  teeth  in  the  mouth  and  presenting  under 
the  microscope  other  phenomena  of  caries  to  be  described  later. 

A  more  prolonged  fermentation  resulted  in  the  complete  disintegra- 
tion of  the  slabs  of  dentine,  a  proof  of  the  fact  that  one  organism 
may  completely  destroy  dentine. 

In  the  tube  containing  only  the  extract  of  beef  no  acid  was  pro- 
duced, and  no  decalcification  of  the  dentine  occurred. 

From  these  facts  Miller  argued  that  putrefaction  does  not  initiate 
the  process  of  dental  caries,  and  may  not  be  essential  to  the  destruc- 
tion of  either  the  inorganic  or  organic  dental  elements. 

Fig.  277. 


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^oo. 


9.  That  the  acid  produced  was  lactic  acid  Miller  demonstrated  as 
follows : 

Starch  and  saliva  were  mixed  and  fermentation  induced.  This  was 
then  checked  by  sterilization  with  heat.  A  quantity  of  material  being 
collected  in  this  manner,  the  whole  was  concentrated  by  evaporation 
and  tested  with  a  solution  of  methyl  \'iolet,  which  would  turn  first 
blue  and  then  green  ^-ith  an  inorganic  acid.  Not  so  reacting,  and  not 
distilHng  off  during  the  concentration,  the  acid  present  was  pronounced 
a  non-volatile  organic  acid.  The  concentrate  was  shaken  with  a 
quantity  of  ether,  which  dissolved  the  organic  acid  present.  When 
the  solution  was  clear  it  was  filtered  and  the  ether  partially  distilled 
off,  when  the  partially  concentrated  solution  was  further  concentrated 
over  a  water  bath  and  then  mixed  with  an  excess  of  freshly  prepared 
zinc  oxide.  The  whole  was  boiled,  water  being  added  as  needed, 
until  the  solution  became  neutral,  when  it  was  set  aside  to  crystallize. 


HISTORY  AND  EXCITING  CAUSES. 


283 


Fig.  278. 


A  drop  placed  upon  a  slide  under  the  microscope  showed  the  forms 
of  crystals  of  zinc  lactate  (Fig.  278). 

By  testing  the  molecular  weight  of  the  washed  and  dried  crystals 
it  was  determined  clearly  that  the  substance  was  zinc  lactate. 

In  practically  a  similar  manner  lactic  acid  was  obtained  directly 
from  carious  dentine. 

While  Miller  demonstrated  the  ability  of  one  organism  to  produce 
all  the  essential  phenomena  of  caries,  including  liquefaction  of  the 
dentine,  he  did  not  claim  that  only  one  or  two  organisms  are  involved 
in  the  process,  but  that  "any  germs  possessing  the  power  of  producing 
acid  fermentation  of  food  may  and  do  take 
part  in  the  first  stage  of  caries,  and  that  all 
those  possessing  a  peptonizing  or  digestive 
action  upon  albuminous  substances  may  take 
part  in  the  second  stage;  and  that  those  pos- 
sessing both  properties  may  take  part  in  both 
stages.  "^ 

Out  of  eighteen  mouth  bacteria  examined 
Miller  found  ten  that  produced  lactic  acid 
in  sugar-containing  solutions.^ 

Hinkins  and  Acree,^  in  experiments  upon 
pure  cultures  of  a  number  of  oral  bacteria  in  various  artificial  media, 
found  lactic,  butyric,  valerianic,  formic,  carbonic,  and  hydrosulphuric 
acids  as  either  principal  or  by-products  of  the  fermentation. 

It  is  quite  clear  from  Miller^s  demonstrations  that  bacteria,  or  at 
least  one  bacteriurn,  are  the  exciting  causes  of  dental  caries;  and  that 
for  their  function  as  such  they  require  carbohydrate  material  as  food. 

Their  action  upon  these  substances  has  been  studied.  The  carbo- 
hydrates introduced  into  the  mouth  as  food  are  monosaccharids, 
diasaccharids,  and  polysaccharids.  (1)  The  monosaccharids  or 
glucoses  have  the  general  formula  CgH,20g  and  are  represented  by 
dextrose  and  levulose,  found  in  fruits,  honey,  and  in  some  forms  of 
so-called  molasses  candy,  and  galactose  formed  from  lactose  or  milk 
sugar  by  hydrolysis.  These  ferment  directly  into  lactic  acid  without 
formation  of  gas.     CgHj^Og  +  bacterial  ferment  =  2C3Hg03. 

A  certain  proportion  of  the  glucose,  etc.,  is  appropriated  by  the 
bacteria  as  food.  (2)  Disaccharids  or  saccharoses  have  the  general 
formula  C12H22O11.     The  principal  one  is  saccharose  found  in  sugar- 


^  Micro-organisms  of  the  Human  Mouth. 
3  Dental  Cosmos,  1901. 


Ibid. 


284  DENTAL  CARIES. 

cane,  the  sugar-beet,  sugar-maple,  and  maize.  This  is  inverted  by 
the  ferment  of  the  bacteria  into  glucose  and  levulose  through  a  process 
of  hydration :     C^HjaOa  +H2O  +B.  ferment  ==  CoH,,,Og  +  CoHiaOo. 

Two  other  disaccharids  enter  the  mouth  or  are  formed  therein: 
lactose  and  maltose,  both  CiaHgaOn +H2O. 

Lactose  exists  in  milk  and  by  hydrolysis  is  changed  to  galactose, 
CgHjgOg,  and  then  ferments  like  other  monosaccharids. 

Maltose  is  an  intermediate  product  in  the  formation  of  glucose  from 
starch. 

(3)  Polysaccharids  or  amyloses  with  the  general  formula  (CgHjgOJn. 
Starch,  cellulose,  glycogen  and  gum. 

Starch  was  found  by  Miller  not  to  undergo  direct  fermentation  by 
mouth  bacteria — i.  e.,  culture  media  containing  starch  but  not  sugar 
M'hen  infected  by  bacteria  did  not  ferment  into  lactic  acid  unless 
ptyalin  was  present.^  When  saliva  was  used,  however,  the  acid  reaction 
occurred,  owing  to  the  formation  of  glucose  through  the  action  of 
ptyalin. 

In  oral  fermentation  starch  is  first  changed  to  maltose  by  hydration; 
the  maltose  to  glucose  and  levulose  and  these  to  lactic  acid: 

starch.  Water.  Ptyalin.  Maltose. 

C^H^^O,,  +  H2O  =  2C,H,20,  (=  4C3H,03). 

Miller  has  demonstrated  that  bacteria  produce  acid  from  starches 
and  sugars  in  about  equal  proportions,  provided  the  starches  are 
cooked.  The  following  synopsis  of  experiments^  made  with  food 
mixed  w^ith  saliva  in  definite  quantities  speaks  fof  itself: 

Material:  Duration  of  Experiment.        Acid  Formed,  in  Units.^ 

Bread,  starch,  potato,  maccaroni, 

rice,    corn,    and    other   cooked 

starches 12  and  30  hours.  20  to  25  and  42  to  110. 

Raw  starches,  potato,  spinach,  etc.  "  "       "  0  0. 

Cane-sugar  and  grape-sugar .  .  "  "       "  17  to  20  and  37  to    41. 

Meats,  fish,  eggs,  etc.  ..."""  0  or  alkahne. 

The  table  shows  that  albuminous  materials  and  raw  starches 
produce  no  acid  and  are  not  concerned  in  caries  except  in  so  far  as 
meats,  etc.,  act  as  culture  media  perpetuating  bacteria  which  later 
may  produce  an  acid  reaction  in  carbohydrate  materials. 

That  alkalies  do  not  produce  tooth  disintegration  in  the  mouth  is 

1  American  System  of  Dentistry,  vol.  i.  pp.  805. 
"  Micro-organisms  of  the  Human  Mouth. 

'  An  acid  unit  equals  the  amount  of  acid  necessary  to  neutralize  0.1  c.cm.  of  a  0.5  per  cent, 
solution  of  potassium  hydrate — i.  e.,  0.5  c.cm.  used  equals  five  acid  units. 


PREDISPOSING  CAUSES.  285 

shown  by  the  fact  that  a  tooth  is  not  affected  by  alkaline  solutions 
which  are  not  strong  enough  to  injure  the  soft  parts. 

The  influence  of  carbohydrate  diet  in  the  production  of  caries  is 
well  shown  by  tables  compiled  by  Mummery  and  quoted  by  Miller/ 
The  races  consuming  a  fish  and  meat  diet  almost  exclusively — e.  g., 
the  Esquimaux — are  recorded  as  having  about  3  per  cent,  of  caries 
in  skulls  examined,  while  those  using  a  mixed  or  vegetable  diet  have 
from  10  to  40  per  cent,  of  caries.  A  most  convincing  example  is 
that  given  by  Miller"  of  two  related  tribes  living  on  either  side  of 
the  Andes  in  the  Argentine  Republic  and  Chili,  respectively.  The 
former,  a  cattle-breeding  and  meat-eating  tribe,  were  practically  free 
from  caries,  while  the  latter,  living  on  mixed  foods  and  consuming 
sugar,  had  19  per  cent,  of  caries. 

While  the  mode  of  action  of  the  causes  of  caries  is  properly  to  be 
considered  under  the  pathology  of  the  disease,  it  may  be  stated,  as 
necessary  to  an  understanding  of  the  predisposing  causes,  that  fungi 
existing  in  the  food  masses  in  the  mouth,  finding  in  the  oral  fluids 
conditions  suited  to  such  an  action,  form  an  exudate  which  may  be 
spoken  of  as  gelatinous  and  which  attaches  the  bacteria  to  each  other 
and  to  the  surface  of  the  enamel.  In  this  situation  carbohydrates 
are  appropriated  as  food  and  lactic  acid  is  produced  in  situ  against 
the  enamel  rods  and  later  against  the  walls  of  the  dentinal  tubules. 

These  "microbic  plaques,"  as  they  have  been  termed  by  Black, 
are  active  only  at  spots  sheltered  from  friction  or  neglected. 

The  Predisposing  Causes  of  Caxies.  It  is  evident  that  the  exciting 
causes  of  caries  act  only  when  the  several  factors  of  fungi,  carbo- 
hydrates, and  spots  sheltered  from  friction  are  combined.  These 
factors  are  so  constantly  present  in  the  human  mouth  that  caries  is 
one  of  the  most  constantly  encountered  diseases  at  the  present  day. 
At  the  same  time  great  differences  are  observed  in  different  individuals 
as  to  the  nature,  extent,  and  rapidity  of  progress  of  caries.  The  extreme 
examples  of  this  are,  on  the  one  hand,  individuals  who  go  through 
life  with  little  or  but  ordinary  care  of  the  teeth,  yet  with  practically 
no  caries,  and,  on  the  other  hand,  those  who  only  by  constant  care 
and  dental  service  are  able  to  check  its  ravages.  These  are  evidently 
conditions  of  immunity  or  predisposition. 

The  causes  of  the  predisposition  to  caries  are  local  or  general. 

Local  Predisposing  Causes.  So  invariably  does  caries  begin 
in  sulci  or  pits  upon  proximal   surfaces  and   unclean   surfaces  that 

'  Micro-organisms  of  the  Human  Mouth.  -  Ibid. 


286  DENTAL  CARIES. 

faults  of  form,  nature  of  approximation,  and  faulty  position  of  the 
teeth  must  bear  a  relation  to  the  diflBculty  of  keeping  the  parts  free 
from  accumulations  of  bacteria  and  carbohydrates. 

These  local  predisposing  causes,  as  they  are  called,  are  simply  con- 
ditions favoring  the  formation  of  the  bacterial  plaques  upon  the  teeth. 

Faults  of  Form.  Deep  pits  or  sulci  in  the  occlusal  surfaces  of 
bicuspids  or  the  occlusal  or  buccal  surfaces  of  molars,  or  in  the  lingual 
surfaces  of  incisors,  and  occasionally  cuspids  or  pits  upon  the  cusps 
of  bicuspids  or  molars,  or  in  other  unusual  situations,  are  not  sub- 
jected to  a  cleansing  friction,  and  so  permit  bacteria  to  form  plaques 
in  these  locations. 

The  nature  of  the  proximal  contact  has  to  do  with  the  inception 
of  caries.  Teeth  are  seen  in  which  the  proximal  surfaces  are  well 
rounded  and  their  buccal  and  lingual  angles  free  from  approximation. 
Such  teeth  are  usually  relatively  narrow  at  their  cervices,  so  that 
these  also  recede  well  from  the  line  of  contact.  A  V-shaped  space 
is  formed  which  the  gum  festoon  normally  nearly  fills.  Such  per- 
fection of  contour  is  also,  as  a  rule,  associated  with  a  perfect  organ- 
ization of  the  enamel  structure  in  virtue  of  which  the  surface  is  smooth. 

While  such  teeth  may  decay  proximally  there  is  much  less  tendency 
to  caries. 

Opposed  to  this  proximations  exist  of  a  broad  nature.  Broad 
proximations  are  very  common  and  not  infrequently  are  associated 
with  a  certain  degree  of  enamel  opacity  and  an  unevenness  of  enamel 
surface  plainly  visible  to  the  naked  eye. 

The  fluid  exuded  by  the  gum  is  normally  alkaline  in  character 
and  probably  neutralizes  the  products  of  acid  fermentation.  In  view 
of  this  fact  the  first-mentioned  form  of  contact  evidently  affords  more 
of  this  immunizing  principle.  The  carrying  of  cavity  margins  beneath 
the  gum  has  been  strongly  indicated  by  experience  as  good  practice 
and  probably  is  explainable  upon  the  same  ground. 

With  the  narrow  approximations  saliva  is  readily  forced  between 
the  teeth  and  neutralizes  the  acids  formed,  or  washes  away  soluble 
carbohydrates,  the  food  for  the  bacteria.  With  the  broad  prox- 
imations such  a  result  is  less  likely  to  occur. 

Miller  has  found  bacterial  plaques  upon  both  carious  and  non- 
carious  teeth  at  the  points  of  approximation,  and  claims  that  the 
carbohydrate  masses  are  the  agents  most  at  fault.  It  is  probable, 
however,  that  the  plaques  plus  the  carbohydrates  are  the  determining 
factors. 


PREDISPOSING  CAUSES.  287 

A  depressed  proximal  surface  may  decay,  but  frequently  does  not. 
An  acquired  fault  of  form  requires  notice. 

Anatomically  the  gum  covers  the  cementum  and  the  enamel  margin. 
When  recession  of  the  gum  occurs,  the  cementum  is  left  exposed  and 
food  debris  accumulates  at  the  angle  formed  by  it  ^dth  the  gum. 
Owing  to  the  cementum  being  less  smooth  than  enamel  microbic 
plaques  readily  collect,  hence  decay  of  the  cementum  frequently 
occurs.     (See  Figs.  28G,  287,  and  '290.) 

Arrangement  ant)  Position  of  the  Teeth.  The  overlapping 
of  one  tooth  upon  another  creates  a  form  of  contact  producing  a 
tendency  to  decay  at  that  point.  Angle^  claims  to  have  observed  a 
comparative  freedom  from  caries  of  very  irregular  teeth. 

The  presence  of  a  supernumerary  third  molar  l}"ing  at  the  buccal 
side  of  the  interdental  space  between  the  second  and  third  upper 
molar  or  an  inlocked  bicuspid  very  frequently  causes  proximal  caries 
at  the  contact  points.  The  upper  third  and  lower  third  molar  frequently 
stand  in  bad  relation  to  the  cheek  or  the  gum. 

Food  collects  upon  their  buccal  surfaces  or  they  are  not  subjected 
to  the  friction  of  the  toothbrush,  and  decalcification  of  a  broad  area 
of  a  buccal  surface  frequently  results. 

Other  Local  Predisposing  Causes.  Acids  taken  in  excess  into 
the  mouth  may  act  as  predisponents  by  causing  a  roughness  of  the 
enamel,  which  invites  the  formation  of  the  bacterial  plaques.  A 
course  of  tincture  of  ferric  chloride  has  a  bad  reputation  in  this  con- 
nection. In  the  cases  observed  by  the  editor  the  hydrochloric  acid 
in  the  tincture  seemed  to  have  formed  roughnesses  between  the  teeth, 
and  many  large  cavities  of  not  unusual  form  were  produced  and 
evidently  due  to  the  carious  process. 

The  acid  vomitus  of  pregnancy  and  seasickness  have  an  analogous 
effect.  It  is  not  likely,  however,  that  during  a  transatlantic  voyage 
large  cavities  can  develop.  The  probable  explanation  of  the  presence 
of  such  cavities  directly  after  the  voyage  is  that  they  existed  before 
the  voyage  was  begun.     (See  Prophylaxis  of  Caries.) 

Under  conditions  of  oral  irritation  such  as  catarrhal  stomatitis,  or 
even  the  presence  of  many  cavities  of  decay,  a  stringy,  mucinous  con- 
dition of  the  saliva  may  result.  This  may  be  due  to  a  partial  coagula- 
tion of  the  mucin  by  the  acid  present  in  the  mouth,  and  the  coagulum 
may  entangle  food  masses  and  cause  their  adherence  to  the  teeth. 

1  Dental  Cosmos,  1903. 


288 


DENTAL  CARIES. 


I  have  shown^  that  acid  appears  in  a  mouth  within  twenty  minutes 
after  a  meal  and  after  the  mouth  has  been  neutrahzed  with  sodium 
bicarbonate  sohition.  It  does  not  readily  appear  if  the  mouth  has 
been  thoroughly  sterilized  with  potassium  permanganate. 

A  lack  of  oral  hygiene  can  hardly  be  considered  a  predisponent  to 
caries,  as  it  introduces  the  exciting  cause,  yet  it  favors  the  retention 
of  food  masses  about  teeth  otherwise  competent  to  care  for  them- 
selves. 

Insufficient  mastication  lessens  the  friction  necessary  to  the  cleanli- 
ness of  the  teeth  and  health  of  the  gums. 

It  is  possible  that  the  secretion  from  the  gum  may  in  some  cases 
be  acid  and  favor  the  production  of  caries  by  decalcifying  the  enamel 
about  the  cervix  (Fig.  279). 

Fig.  279. 


Caries  of  enamel  about  the  cer-vaces  of  many  teeth,  due  to  tenacious  films  collected  upon 
them;  at  first  probably  neglected,  later  impossible  to  cleanse  \\dth  brush  alone.  Model  by 
AV.  A.  Capon. 

The  structure  of  the  enamel  has  no  relation  to  the  inception  of 
caries.  A  roughness  of  the  enamel  surface  may  act  as  a  favoring 
condition,  and  after  inception  of  caries  inferior  structure  and  possibly 
the  presence  of  Caush's  tubes  may  permit  more  rapid  disintegration. 
(See  p.  141.)  An  interesting  examination  of  16,000  mouths  made 
in  Sweden  by  Forberg  (Stockholm)  and  others  by  Rose  in  Baden  and 
Thuringia  seem  to  show  that  there  is  a  relation  between  the  color 
(structure)  of  teeth  and  the  presence  of  caries,  the  following  averages 
of  all  ages  being  observed:  white  teeth,  14.3  per  cent,  of  caries; 
yellowish-white,  16.4  per  cent.;  yellow,  20.0  per  cent.;  grayish-blue, 
24.3  per  cent. 

According  to  these  observers,"  in  the  regions  in  which  the  water  was 
rich  in  calcium  salts  the  individuals  examined  had  the  yellowish-white 
teeth. 

1  Dental  Cosmos,  1899.  -  Ibid.,  1901. 


PREDISPOSING  CAUSES.  289 

General  Predisposing  Causes.  Some  individuals  seem  to  suffer 
much  from  caries,  others  in  less  degree.  In  either  case  periods  of 
immunity  or  comparative  immunity  may  be  established  and  may 
be  again  followed  by  a  period  of  susceptibility  and  a  succeeding 
immunity. 

Black^  made  analyses  of  so-called  hard  and  soft  teeth  and  deduced 
from  them  the  opinion  that  the  hardness  and  softness  of  teeth  have 
nothing  to  do  with  the  inception  of  caries. 

Touching  this  point  Black^  instances  the  case  of  a  man  whose 
enamel  had  always  been  chalky  and  as  easily  cut  as  a  slate-pencil, 
yet  who  had  little  caries  of  the  teeth.  That  some  teeth  of  apparently 
poor  structure  and  defective  form  do  not  decay  is  also  a  fact  of  common 
observation. 

These  facts  point  to  the  conclusion  that  a  period  of  caries  is  due 
either  to  a  temporary  lack  of  oral  hygiene  with  a  corresponding 
intensity  in  oral  fermentation^^/,  e.,  the  exciting  cause  is  active — or 
that  it  is  due  to  some  systemic  condition  which  changes  the  constitution 
of  the  oral  fluids,  permitting  the  formation  of  the  microbic  plaques 
upon  the  teeth. 

Black  has  shown  that  caries  fungi  are  always  present  in  the  mouth, 
but  do  not  always  form  the  plaques.  Cases  also  exist  in  which  caries 
has  begun  during  some  period  of  susceptibility  and  a  number  of  new 
cavities  have  been  started.  Later  a  period  of  immunity  has  followed 
and  the  cavities  have  not  progressed. 

So  far  as  classed,  systemic  conditions  influencing  susceptibility  and 
immunity  may  be  placed  under  the  four  headings:  Heredity,  Pre- 
natal and  Postnatal  Influences,  Age,  and  Bodily  Condition. 

Heredity.  The  children  of  parents  whose  teeth  decay  readily  seem  to 
be  subject  to  caries  in  marked  degree.  When  one  parent  is  immune 
the  child  may  resemble  one  or  the  other  in  this  respect. 

Black^  records  observations  on  certain  families  as  showing  a  tendency 
to  caries  of  certain  teeth  at  a  given  age,  or  in  certain  positions  upon 
the  teeth — e.  g.,  occlusal  pits.  In  certain  cases  the  hereditary  tendency 
persists  throughout  life. 

Faults  of  form  and  position  contributing  to  the  inception  of  caries 
may  be  considered  as  direct  inheritances  or  results  of  inherited  disease 
or  physical  tendencies.  The  inherited  tendency  to  caries  may  be  due 
to  an  inherited  general  modification  of  cell  physiology  which  permits 
the  development  of  caries  fungi  and  their  plaques. 

1  Dental  Cosmos,  May,  1895.  "-  Ibid.,  June,  1898.  ^  ibid.,  1899. 

19 


290  DENTAL  CARIES. 

Prenatal  and  Posfnatal  Influences.  It  is  quite  possible  that  the 
systemic  condition  of  the  mother  during  gestation  may  profoundly 
modifv  the  anatomicophysiological  condition  of  the  body  cells  of  the 
child ;  nutritional  processes  may  suffer  and  the  postnatal  tooth  develop- 
ment proceed  irregularly,  structure  being  affected;  moreover,  the 
altered  biochemical  function  of  the  cells  may  stand  in  close  relation 
to  the  constitution  of  the  oral  fluids,  and  these  in  turn  may  favor  the 
development  of  caries  fungi.  The  same  line  of  argument  may  be 
applied  to  bottle  feeding  of  recently  born  infants,  or  to  other  con- 
ditions profoundly  affecting  general  nutrition. 

In  an  examination  of  school-children  Th.  Frick^  (Zurich)  found  a 
much  greater  percentage  of  decay  in  children  that  had  been  bottle 
fed  at  between  three  and  six  months  of  age.  He  performed  an  experi- 
ment on  a  litter  of  six  dogs,  feeding  three  on  cows'  milk  and  bouillon ; 
one  of  them  died  and  the  others  had  poorly  developed  teeth.  The 
controls  were  normal. 

Forberff  and  Rose^  have  shown  that  the  individuals  who  drink 
water  rich  in  calcium  salts  have  a  smaller  percentage  of  caries  than 
those  drinking  soft  waters.  Whether  this  effect  is  due  to  a  better 
development  of  tooth  structure  or  is  a  postdevelopmental  effect  is  not 
stated.  Degeneracy  must  be  considered  as  a  factor  possibly  in- 
fluencing the  body  cells. 

Age.  That  the  age  has  an  influence  upon  caries  was  noted  by 
Flagg.  He  recorded  the  ages  from  five  to  eight,  twelve  to  twenty, 
thirty  to  thirty-five,  forty-five  to  fifty,  sixty  to  sixty-five,  and  senility 
as  periods  of  decay,  while  the  intervening  periods  were  intervals  of 
comparative  exemption. 

Black  has  noted  that  caries  is  a  disease  of  youth,  most  intense 
before  adult  age,  at  which  time  immunity  is  established,  provided  the 
teeth  have  been  well  and  promptly  filled  and  the  mouth  otherwise 
cared  for.  In  view  of  this  fact  he  aims  at  establishing  this  immunity 
by  close  attention  to  the  teeth  during  youth. 

He  records  fluctuations  in  susceptibility  not  unlike  those  recorded 
by  Flagg,  and  also  points  out  that  some  persons  pass  through  the 
ordinary  periods  of  susceptibility  and  first  develop  caries  in  middle 
age.  In  old  age  general  recession  of  the  gum  is  common,  and  in  the 
conditions  of  debility  associated  with  old  age  much  caries  of  cementum 
occurs.  So  far  as  I  have  observed  such  cases  it  seems  that  the 
oral  fermentation   is  more  intense  than    at    other   periods,  microbic 

1  Dental  Cosmos,  1901.  i  Ibid.,  1899. 


PREDISPOSING  CAUSES.  291 

plaques  form,  and  the  tissue  attacked  is  less  resistant  to  decalcifying 
agents.  Moreover,  the  patients  are  either  unwilling  or  unable  to  keep 
the  cementum  cleansed. 

Repeated  examinations  of  the  mouths  of  school-children  show  a 
deplorable  amount  of  caries  which  may,  perhaps,  be  attributable  to 
several  causes,  such  as  the  induction  of  a  lessened  systemic  resistance 
due  to  confinement,  study,  etc.,  and  also  to  the  inhalation  of  vitiated 
air,  which  presumably  also  contains  acid-producing  bacteria.  More- 
over, bacteria  of  caries  may  be  directly  transmitted  by  kissing,  common 
use  of  pencils,  etc. 

Michaels,^  of  Paris,  has  observed  that  "the  saliva  of  adolescence 
contains  a  dextrinic  principle  (glycogen)  susceptible  of  fermentation 
under  the  influence  of  ptyalin  in  the  presence  of  earthy  salts.  Lactic 
acid  is  formed." 

Bodily  Condition.  It  is  a  matter  of  observation  that  such  conditions 
as  pregnancy,  typhoid  fever,  anaemia,  leukgemia,  diabetes,  dyspepsia, 
and  debility  are  frequently  accompanied  by  or  followed  by  a  devel- 
opment of  cavities  of  decay,  but  whether  the  diseases  themselves  or 
a  coincident  lack  of  oral  hygiene  act  to  permit  the  formation  of  the 
gelatinous  plaques  has  not  clearly  been  made  out.  If  oral  and  dental 
prophylaxis  be  practised  during  typhoid  fever  and  convalescence 
therefrom,  the  production  of  cavities  is  much  limited,  but  this  does 
not  prove  anything.  The  same  is  true  of  pregnancy,  which  introduces 
an  exciting  cause  (the  vomitus),  and  of  glycosuria,  which  introduces 
glucose.  Black  contends  that  periods  of  susceptibility  are  noted 
both  in  apparent  good  and  ill  health.  That  apparent  health  may 
really  not  be  true  health  is  a  matter  that  must  be  considered. 

Michaels^  states  that  the  constitution  of  the  saliva  changes  with 
the  establishment  of  various  diatheses,  and  that  a  physiological 
saliva  with  the  biochemical  principles  in  a  state  of  equilibrium  is 
probably  very  rare.  The  exact  findings  of  Michaels  have  not  as  yet 
satisfactorily  explained  the  influence  of  the  change  in  saliva  upon 
the  production  of  dental  caries  as  commonly  seen.  He,  however, 
states  that  the  most  active  dental  caries  is  found  in  the  mouths  of 
hypo- acid  individuals. 

That  such  a  change  may,  however,  favor  or  retard  the  growth  of 
caries  fungi,  according  to  the  nature  of  the  change,  is  quite  evident 
and  may  yet  be  shown  to  be  the  predisposing  cause  hinted  at  by 
Black. 

^  Sialosemeiology.     See  Dental  Cosmos,  1900.  ^  Ibid,  December,  1900. 


CHAPTER   XIII. 


DENTAL  CARIES:    PATHOLOGY,  MORBID  ANATOMY,  AND 
CLINICAL  HISTORY. 

PATHOLOGY  AND  MORBID  ANATOMY. 

It  is  a  fact  of  common  observation  that  caries  begins  only  at 
spots  protected  from  friction  or  imcleansed.  These  are  in  order  of 
frequency:  (1)  pits,  grooves,  and  fissures  in  the  enamel;  (2)  proximal 
surfaces  just  above  the  contact  points;  (3)  smooth  surfaces  which 
from  any  cause  are  habitually  unclean;  (4)  necks  of  the  teeth  at  or 
near  the  junction  of  the  cementum  and  enamel  (Black). 


Fig.  280. 


Fig.  285. 


Fig.  291. 


Fig.  281. 


Fig.  282. 


Fig.  286. 


Fig.  289. 


Fig.  292. 


Fig.  283. 


Fig.  284. 


Fig.  290. 


In  these  situations  Williams  has  demonstrated  the  fact  that  the  oral 
bacteria,  protected  from  friction,  attach  themselves  to  the  enamel, 
forming  microbic  plaques  which  are  sufficiently  adherent  to  permit 
their  retention  during  the  grinding  of  the  specimen  f6r  microscopic 
examination.     (See  Figs.  294,  295,  and  296.) 


PATHOLOGY  AND  MORBID  ANATOMY. 


293 


Black  has  stated'  that  "the  formation  of  gelatinous  plaques  does 
not  occur  in  every  mouth,  though  the  caries  fungi  do  grow  in  all 
mouths,  and  that  in  the  growth  of  the  caries  fungus  on  artificial  media 
it  tnay  be  made  to  produce  a  gelatinous  material  or  grow  without 
forming  it  by  manipulation  of  the  culture  medium.  The  gelatinous 
plaque  is  a  thin,  transparent  film,  usually  escaping  observation,  and  is 
not  the  materies  alba  nor  sordes." 

Fig.  294. 


Section  of  normal  human  enamel,  showing  thick,  felt-like  mass  of  micro-organisms  slightly 
raised  from  the  surface  of  the  tissue  by  pressure  of  the  cover-glass  in  mounting.  X  350. 
(Williams.) 

Goadby^  has  succeeded  in  obtaining  mucinous  plaques  upon  steril- 
ized teeth  suspended  in  cultures  of  staphylococcus  viscosus  in  non- 
carbohydrate  media.  He  has  found  this  organism  upon  the  white 
decalcified  surfaces  of  enamel  in  the  mouth.^ 

In  the  plaques  are  bacteria  of  many  kinds,  including  thread  forms, 
and  they  form  a  thick,  felt-like  mass  always  present  at  spots  of  enamel 
undergoing  decay.  In  these  situations  Williams^  has  invariably  found 
the  leptothrix  racemosa  of  Vicentini,  a  mould-like  fungus.  Its  relation 
to  caries  is  not,  however,  certain  (Figs.  297  and  298). 


1  Dental  Cosmos,  September,  1899. 
3  Ibid. 


-  Mycology  of  the  Mouth. 
*  Dental  Cosmos,  1897. 


294 


DENTAL  CARIES. 


The  bacteria  in  the  pkiques  require  food  and  obtain  it  from  the 
carbohydrate  and  albuminous  materials  which  come  in  contact  with 
them.  From  the  carbohydrates  lactic  acid  is  produced  as  a  waste 
product.  (See  Chapter  XII.)  Williams  states  that  it  is  "  highly  improb- 
able that  the  enamel  is  affected,  except  in  rare  and  special  instances, 
by  any  other  acid  than  that  which  is  being  excreted  by  the  bacteria 
at  the  very  point  at  which  they  are  attached  to  the  enamel." 


Fig.  295. 


Micro-organisms  of  caries  attached  to  enamel  on  approximal  surface  of  tooth.     (WilHams.) 

This  thick,  glutinous-like  mass  of  fungi  also  prevents  the  excreted 
acid  from  being  washed  away,  so  that  it  exerts  its  full  chemical  power 
upon  calcific  tissue. 

The  lactic  acid  produced  attacks  the  inorganic  matter  of  the  enamel, 
following  first  the  interprismatic  cement  substance  between  the  prisms, 
later  dissolving  the  transverse  cement  substance  between  the  globules. 


PATHOLOGY  AND  MORBID  ANATOMY. 

Fig.  296. 


295 


Superficial  approximal  caries  of  enamel  with   films;   also   shows  shght   approximal 
abrasion.     (Miller.) 

Fig.  297 


Budding  of  spores  on  the  stems  of  leptothrix  racemosa.     (Williams.) 


296 


DENTAL  CARIES. 


The  effect  is  to  produce  an  irregular,  roughened  surface  of  the  enamel 
and  to  bring  into  view  the  structure  of  the  rods  (Fig.  301). 

The  gradual  loss  of  cement  substance  unbinds  the  enamel  globules, 
which  are  in  turn  dissolved  and  washed  away,  leaving  a  depression 
or  cavity. 

In  the  process  of  enamel  dissolution  the  bacteria  may  enter  the 
crevices  formed  by  solution  of  the  interprismatic  cement  substance 
and  by  repetition  of  the  process  gain  access  to  the  dentine  (Fig.  304). 


Fin.   298. 


Thi(.-k  growth  of  leptothrix  racemosa  fructification  heads  from  approximal  surface  of  tooth, 
under  high  magnifying  power.     (Williams.) 


The  form  of  the  enamel  may  be  retained  until  and  even  after 
decalcification  has  reached  the  dentine.  Clinically  this  is  seen  as  a 
discolored  spot,  resisting  the  instrument  until  some  force  is  used,  when 
it  rapidly  breaks  down. 


PATHOLOGY  AND  MORBID  ANATOMY 


297 


Fig.  299. 


,.:-   \ 


A  form  of  streptococcus  found  abundantly  in  mouths  where  very  rapid  decay  of  the  teeth 
is  in  progress.     X  750.     (Williams.) 

Ftg.  300. 


Scrapings  of  micro-organisms  from  the  approximal  surface  of  a  decaying  tooth:  shows  the  lepto- 
thrix  bucealis  maxima  and  the  bacillus  buccalis  maximus  of  Miller.    X  1500.    (Williams.) 


298 


DEXTAL  CARIES 


It  is  also  noted  clinically  and  microscopically  that  the  decalcification 
is  deepest  at  a  spot  just  above  the  point  of  contact,  and  less  deep  at 
points  buccal  or  lingual,  occlusal  or  cervical,  to  this  spot,  and  still  less 
at  points  more  buccal  or  lingual — /.  e.,  it  shades  off  to  zero  lingually, 
buccally,  occlusally,  and  cervically  (Figs.  296  and  305). 

The  dentine  may  in  such  cases  be  deeply  affected.  When  the  entire 
thickness  of  the  enamel  is  penetrated  and  the  dentine  attacked,  there  is 


Fig.  301. 


Section  through  human  enamel,  showing  first  stages  of  caries — i.  e.,  solution  of  interprismatic 
cement, substance.     To  be  compared  with  Fig.  183.     (Williams.) 


a  change  in  the  mode  of  progress  of  the  decalcification,  which  pro- 
ceeds along  the  line  of  union  between  the  enamel  and  dentine,  as 
well  as  directly  into  the  dentine  (Fig.  305)  ;  in  this  way  the  enamel  is 
attacked  from  its  dentinal  side  (Fig.  303).  Bacteria  growing  in  the 
spaces  from  which  the  interprismatic  cement  substance  has  disappeared 
cause  detachment  of  masses  of  partially  decalcified  rods  (Fig.  306). 

In  the  ultimate  breaking  down  of  the  enamel  the  rods  first  separate ; 
the  outlines  of  the  several  globules  of  which  the  rods  are  composed  are 


PATHOLOGY  AND  MORBID  ANATOMY 


299 


brought  into  plain  view;  next,  the  calcified  plasmic  strings  noted  in 
enamel  formation  become  evident;  and  finally  the  bead-like  masses 
upon  these  strings  are  left  as  the  ultimate  granular  detritus  of  the 
enamel. 

In  cases  of  rapid  enamel  dissolution  Williams  found  streptococci 
almost  invariably  present;  and  suggests  tentatively  that  the  variety  of 
organisms  may  be  the  factor  governing  the  rapidity  of  dissolution 
(Fig.  299). 


Fig.  302. 


Section  of  human  bicuspid,  showing  commencement  of  caries;  a  and  a',  appearances  caused 
in  enamel  and  dentine  by  the  acid  of  decay;  b  and  &-,  shreds  of  a  felt-like  mass  of  bacteria  raised 
from  the  surface  of  the  enamel;  c,  a  cavity.     X  12.     (Williams.) 


These  are  probably  the  streptococcus  brevis  of  Goadby  (micro- 
coccus nexifer  of  Miller). 

Williams  found  S.  pyogenes  albus  and  aureus  and  sarcinea  lutea 
to  be  acid  producers. 

The  large  cocci  and  diplococci  shown  in  Fig.  306  were  always 
found  in  the  secondary  decay  of  enamel. 

"In  the  direct  caries  of  enamel  the  cavities  are  lined  with  leptothrix 
and  thread-like  forms"  (Fig.  308). 

"The  leptothrix  buccalis  maxima  and  the  bacillus  buccalis  maximus 
of  Miller  are  nearly  always  found,  the  latter  more  sparingly"  (Fig.  300). 


300 


DENTAL  CARIES. 


"Beneath  the  felt-Uke  masses  of  thread  forms  and  lying  in  contact 
with  the  decomposing  enamel  in  direct  decay,  and  also  in  deep  cracks 


Fir..   303. 


Section  of  carious  tooth,  showing  aiijiearances  of  decay  in  enamel  and  dentine  at  the  line  of 
union  of  these  tissues;  the  dark  spots  shown  in  the  enamel  and  dentine  are  masses  of  micro- 
organisms.    X  250.     (Williams.) 


Fig.   304. 


Penetration  of  bacilli  between  enamel  prisms  after  solution  of  interprismatic  cement  substance. 

(MiUer.) 

and  fissures  in  secondary  decay,  there  is  invariably  found  a  short, 
thick  bacillus,  usually  constricted  in  the  centre." 


PATHOLOGY  AND  MORBID  ANATOMY. 


301 


Caries  of  Nasmyth's  Membrane.  Miller^  demonstrated  that  the 
enamel  cuticle  may  act  as  a  breeding  ground  for  many  forms  of  bacteria 
which  occupy  it,  forming  a  matrix  which  may  retain  minute  particles 
of  food,  which  in  turn  aid  in  acceleration  of  the  progress  of  decay 
(Fig.  309). 

Caries  of  Dentine.  The  bacteria  after  penetrating  the  substance 
of  the  enamel  attack  the  dentine.  This  presents  a  different  anatomical 
and  chemical  structure  to  be  acted  upon.     Beneath  the  enamel  the 

Fig.  305. 


Decalcification  of  enamel  without  loss  of  form :  a,  film.      X  35.     (Miller.) 

first  layer  of  dentine  is  of  a  composition  which  permits  the  bacteria 
to  rapidly  spread  laterally  along  this  zone.  They  also  enter  the  tubules 
of  the  dentine  and  penetrate  by  multiplication  toward  the  pulp.  A 
wedge-shaped  area  of  decay  is  produced  (Fig.  311). 

In  all  cases  decalcification  precedes  these  invasions.  At  the  periphery 
the  tubules  communicate  freely  by  their  lateral  branches  (Fig.  310), 
and  the  lateral  spreading  of  the  bacteria  by  multiplication  is  readily 
ej^lained. 


1  Micro-organisms  of  the  Human  Mouth,  1890,  and  Dental  Cosmos,  1900. 


302 


DENTAL  CARIES 


It  is  seen  clinically  in  caries  that  a  portion  of  the  dentine  is  abso- 
lutely destroyed  and  removed,  leaving  within  the  tooth  a  "cavity  of 
decay"  bounded  by  dentine  and  enamel  undergoing  disintegration;  be- 
neath this  lies  dentine  less  affected,  and  beneath  this  sound  dentine 
(Fig.  311).    These  phenomena  require  explanation. 

The  tubules  of  the  decalcified  dentine  become  packed  for  a  distance 
with  bacteria  (Figs.  312  and  314).   These  probably  act  upon  the  organic 


Cover-glass  preparation  from  =c..i,..;,4.  ._,.  ..  .i^.c,  ..,'aqae,  decaying  enamel:  the  cement  sub- 
stance between  the  rods  is  seen  to  be  dissolved  away,  and  the  crevasses  thus  formed  are  filled 
with  round  and  oval  forms  of  micrococci  and  bacteria.  Stained  by  the  Gram  method.  X  450. 
(Williams.) 


matrix  of  the  decalcified  tubule  walls.  The  internal  pressure  due  to 
multiplication  distends  them  so  that  the  lumen  is  enlarged.  At  the  same 
time  the  bacteria  excrete  a  ferment  or  ferments  which  cause  the  wall 
at  first  to  thicken.  The  dilatation  and  thickening  together  cause  the 
compression  of  the  decalcified  intertubular  substance,  and  the  tubules 


PATHOLOGY  AND  MORBID  ANATOMY. 


303 


assume  an  hexagonal  shape  owing  to  the  mutual  pressure.  The 
phenomenon  is  not  a  vital  one,  as  it  occurs  in  artificial  caries  (Miller) . 
(Fig.  313.) 


Fig.   307. 


Various  forms  of  micrococci  and  bacteria  from  decaying  enamel.    Photographed  by  Mr.  Andrew 
Pringle  from  Williams'  cover-glass  preparation.     X  1000.     (Williams.) 


Fig.  308. 


Cover-glass  preparation  of  scrapings  from  decay  of  enamel:  shows  leptothrix  bucealis  maxima 
and  bacillus  bucealis  maximus  of  Miller.    Stained  by  Gram  method.    X  850.    (Williams.) 


304 


DENTAL  CARIES. 


The  bacterial  ferment  possesses  a  digestive  or  peptonizing  power  and 
begins  to  liquefy  the  inner  surface  of  the  tubule  wall.  As  it  tloes  so 
the  lumen  is  further  increased  and  the  bacteria  fill  the  acquired  space. 
Taking  up  carbohydrates  lactic  acid  is  produced,  which  combines  with 


Fig.  309. 


Enamel  cuticle  permeated  by  bacteria.     (1100  :  1.)     (Miller.) 
Fig.  310. 


Carious  dentine,  stained  with  fuchsin  to  show  micro-organisms.  The  section  shows  the  con- 
dition of  the  tubules  as  filled  with  micro-organisms  along  the  junction  of  the  dentine  with  the 
enamel  at  a.     The  tubules  are  very  much  enlarged,     (i/io  immersion  objective.)     (Black.) 

the  calcium  salts  of   deeper  tubules  and  intertubular  substance  and 

prepares  a  path  of  decalcified  tissue  for  bacterial  advance  (Fig.  314). 

This  combination  of  the  acid  with  the  calcium  salts  disposes  of  or 

neutralizes  the  acid,  which,  if  accumulated  to  the  strength  of  0.75  per 


PATHOLOGY  AND  MORBID  ANATOMY. 


305 


cent.,  would  cause  the  destruction  of  the  bacteria  (by  their  waste 
products).  (Miller.)  Calcium  lactophosphate,  calcium  lactate,  and 
magnesium  lactophosphate  are  produced.     (See  p.  258.) 

The  bacterial  ferments  continue  to  digest  the  wall  of  the  tubule 


Fig.  311. 


Longitudinal  ground-section  through  the  crown  of  an  inferior  molar  of  a  negro:  E,  enamel; 
D,  dentine;  C,  cement;  p,  pulp  chamber;  a,  large  decay,  from  the  occlusal  surface;  6,  small 
decay,  from  the  mesal  surface;  C  s,  cone  of  septic  invasion  and  discoloration;  e,  partially  decal- 
cified and  discolored  enamel  around  the  carious  cavity;  z,  dark  cones;  s',  clearer  cones;  s'p, 
oldest  cones  where  putrefaction  of  the  tooth  cartilage  begins;  c,  outer  transparent  zone,  or  zone 
of  Tomes;  s  d,  secondary  dentine,  caused  by  irritation;  s'd',  secondary  dentine  deposited  by  normal 
physiological  process,  recession  of  the  pulp.  This  figure  is  drawn  from  a  ground  and  polished 
section  mounted  in  Canada  balsam.     (Gysi.) 

20 


306 


DEXTAL  CARIES. 


and  a  time  arrives  when  they  have  penetrated  its  substance.  The 
intemibular  substance  is  then  removed  in  Uke  manner.  The  same 
process  occurring  in  adjoining  tubules  as  well,  the  entire  dentinal 


Fte.  312- 


FiG.  313. 


*  ^ 


Ottss-^section    of    deea$«d    dmtiiie:    ibe 
thioogh  leoprocal  piessme  have  assumed  fbe  shspe 
of  5  and  6Haded  pnsms.     (Uilte-.) 

substance  in  the  particular  area  at  the 
cavity  surface  is  destroyed — i.  e.,  Uque- 
fied  and  washed  away    Fig.  311,  ai. 

Occurring  at   a   point    beneath   the 

general  cavity  surface,  the  bacteria  in 

several  adjoining  tubules  destroy  their  walls  and  the  intervening  in- 

tertubular  substance,  forming  what  ^liller  has  called  a  '*  Hquef action 


fiaTim»g  dentme,  blowing  in~ 
Taded  tnboles  and  iminvaded 
bvt  deealdSed  mtatobalar  aib- 


-a:^' 


aesiatSQoi  deeaieaa&a  demidiiie  ptajrlyaii-jnadedby  baciOTa:  a,  nmnfaded  zmk.     (Idte'.) 

focus"  ifpl.  foci).     (Tig.  315.)     This  action  proceeds  imtil  the  enamel 
is  undennined  and  the  pulp  is  exposed. 


PATHOLOGY  AXD  MORBID  AX  ATOMY. 


307 


As  the  enamel  is  undermined  by  the  carious  process  the  bacteria 
and  their  acids  decalcify  its  inner  surface,  the  process  proceeding  from 
within  outward  and  termed  "secondare  caries"  of  enamel. 


Fig.  315 

.A' 


m 


■^;ii^b 


W'i-, 


'm 


Liquefaction  foci.     (Miller.) 

The  enamel  is  thus  weakened  and  at 
the  same  time  deprived  of  dentinal  sup- 
port and  breaks  down  under  stress  of  mas- 
tication. 

Any  interglobular  spaces  in  the  dentine 
being  filled  with  transitional  or  uncalcified 
material  like  the  tubule  walls  are  rapidly 

invaded    by  the    bacteria  during    their   progress    along   the   tubules 
(Fig.  317).' 


Decayed  dentine  showing  a 
mixed  infection  ■with  cocci  and 
bacilli.      •    400.     iMiUer.) 


Fig.  317. 


■'-fM 


vrf  '^^^fffS^J^'fi'/i/ 


Interglobular  spaces  filled  with  bacteria.     Oliller.) 

The  character  of  the  organisms  in  the  tubules  and  the  nature  of 
the  Kquefaction  seem  to  depend  upon  the  particular  germs  present. 


308  DEXTAL  CARIES. 

Miller  has  shown  that  in  the  deeper  portions  of  tubules  micrococci 
appear  to  predominate  over  the  rod  forms,  which  are  also  present; 
although  one  tubule  may  be  filled  with  cocci  and  its  neighbor  with 
rod  forms  (Fig.  316).  It  is  only  in  the  more  superficial  layers  that 
the  thread  forms  are  found  in  numbers. 

Goadby^  has  done  much  interesting  work  in  this  direction  and 
offers  the  following  classification  of  bacteria  found  in  decaved  dentine: 


Bacteria  of  Dental  Cakies. 
Acid-forming  Bacteria. 


Streptococcus  brevis 
B.  necrodentalis 
Staphylococcus  albus 
Streptococcus  bre\'is 
Sarcina  lutea     . 
Sarcina  aurantiaca    . 
Sarcina  alba  (Eisenberg) 
Staphylococcus  albus 
Staphylococcus  aureus 


Deep  layers  of  carious  dentine.     ' 
■  Superficial  layers  of  carious  dentine. 


Bacteria  which  Liquefy  Dentine  (Decalcified). 


None  isolated  as  yet 

B.  mesentericus  ruber 

B.  mesentericus  vulgatus 

B.  mesentericus  fuscus 

B.  fervus  ..... 

B.  gingivae  pyogenes 

B.  Kquefaciens  fluorescens  motilis 

B.  subtilis  .... 

Proteus  Zenkeri 

B.  plexiformis  .... 


Deep  layers  of  carious  dentine. 

1 


i-  Superficial  layers  of  carious  dentine. 


Goadby  states  that  his  experiments  show  that  the  bacteria  which 
dissolve  blood  serum  also  digest  decalcified  dentine,  while  those  which 
only  liquefy  gelatin  do  not  digest  decalcified  dentine. 

His  experiments  also  indicate  that  of  the  bacteria  found  in  the 
superficial  layers  of  carious  dentine  some  produce  digestive  enzymes, 
others  acid  fermentation,  and  others  have  both  functions. 

Choquet^  has  confirmed  the  observation  of  Miller,  Vignal,  Gallipe, 
and  Goadby,  that  the  deeper  the  portions  of  dentine  examined  the 
fewer  species  of  fungi  are  found  in  the  tubules,  and  explains  it  upon 
the  ground  that  the  anaerobic  or  facultative  aerobic  organisms  in  the 
outer  layers  advance  into  the  deeper  dentine  because  they  are  better 
suited  to  the  conditions. 

These  exact  findings  are  interesting  as  bearing  out  the  general 
demonstrations  of  IVIiller;  at  the  same  time,  Miller's  experiment  show- 
ing absolute  dissolution  by  a  single  bacterium  in  pure  culture  is  to  be 
recalled. 

'  Mycology  of  the  Mouth,  and  Dental  Cosmos. 
-  Microbes  of  Dental  Caries,  Dental  Cosmos,  1900. 


PATHOLOGY  AND  MORBID  ANATOMY.  309 

Choquet^  has  shown  that  dental  caries  may  proceed  under  fillings 
against  sound  dentine  by  the  following  experiment: 

Artificial  cavities  were  prepared  in  the  incisors  of  a  sheep.  In  these 
was  securely  sealed  with  cement  a  small  particle  of  a  gelatin  culture  of 
caries  fungi  applied  on  a  sterilized  platinum  cap.  Nine  months  later 
the  dentine  had  become  yellow,  slightly  decalcified,  and  the  tubules  pene- 
trated by  bacteria.  This  softened  dentine  was  used  to  inoculate  a  por- 
tion of  the  medium  originally  used,  and  the  species  again  cultivated. 

Miller^  estimated  the  relative  loss  of  inorganic  and  organic  matter 
in  dentine  during  the  process  of  caries  by  weighing  and  analyzing 
equal  volumes  of  carious  and  sound  dentine  from  the  same  teeth. 

The  carious  dentine  had  lost  about  seven-ninths  of  its  weight, 
twelve-thirteenths  of  its  original  calcium  salts  by  decalcification,  and 
two-fifths  of  its  original  organic  matter  by  liquefaction  of  its  substance. 

Tube  Casts.  In  the  zone  of  decalcification  in  advance  of  bacterial 
invasion  of  the  tubes  are  found  rod-shaped  bodies  or  shining  granules, 
first  described  by  J.  Tomes.  They  occur  in  both  natural  and  artificial 
caries,  hence  it  must  be  inferred  that  their  presence  is  not  the  result 
of  a  vital  process. 

The  rods  do  not  dissolve  in  organic  acids,  but  dilute  sulphuric  acid 
quickly  dissolves  them.  They  are  unaffected  by  alcohol  or  chloroform, 
a  proof  that  they  are  not  composed  of  fat.  Miller 
regards  them  as  probably  calcic  formations  against 
the  tubule  wall  as  a  cast  of  the  wall,  and  which 
become  loosened  when  enlargement  of  the  tubule 
occurs.  They  have  a  tubular  structure,  are  brittle, 
and  may  contain  a  central,  thread-like  filament 
which  may  possibly  be  the  remains  of  a  dentinal 
fibril.  Bacteria  may.  surround  them,  but  do  not 
enter  them.    The  granules  are  probably  broken  rods.^ 

"  r  J  Tube  casts. 

The  data  point  toward  a  probability  that  the  rods 
are  composed  of  calcium  lactate  and  calcium  lactophosphate,  the 
result  of  a  combination  of  the  lactic  acid  with  the  calcium  salts  of 
the  dentine.  The  resultant  salt  is  probably  deposited  as  a  tube  cast, 
as  suggested  by  Miller.  Polariscopic  experiments  should  be  compe- 
tent to  settle  the  question. 

The  Transparent  Zone.  Around  the  zone  of  decalcified  uninfected 
dentine  appears  a  zone  of  dentine  more  transparent  than  the  surround- 

1  Microbes  of  Dental  Caries,  Dental  Cosmos,  1900. 

2  Micro-organisms  of  the  Human  Mouth.  3  Miller 


310 


DENTAL  CARIES. 


ing  normal  dentine.  The  zone  extends  from  periphery  to  periphery 
around  the  cone  of  carious  dentine  (Fig.  311,  c).  The  tubules  in  this 
area  contain  granular  matter  not  seen  in  normal  dentine  nor  in  the 
dentine  of  dead  teeth  in  the  same  situation.^ 

Tomes  and  Magitot  both  regarded  the  transparency  as  an  attempt 
made  by  nature  to  impede  the  progress  of  caries.  Walkhoff  regards 
it  as  due  to  a  sclerotic  action,  the  fibrillre  upon  stimulation  producing 
intercellular  substance  (tubule  wall)  at  their  own  expense  and  primarily 

Fio.  319. 


Section  from  a  lower  incisor  worn  on  a  plate:  extensive  decay  without  increase  of  transparency. 

X  15.      (Miller.) 

of  their  offshoots.     Black  regarded  it  as  the  earliest  stage  of  decalci- 
fication.    Miller  advanced  the  following  data:^ 

1.  Transparency  indicates  increased  homogeneity  as  opposed  to  the 
heterogeneity  of  normal  dentine — i.  e.,  the  coefficients  of  light  refrac- 
tion are  brought  nearer  together. 

2.  It  occurs  in  living  dentine  only  and  is  not  found  in  natural  teeth 
mounted  on  plates  and  decayed  in  the  mouth,  nor  in  secondary  caries 
of  dentine  from  the  pulp  ca^dty  to  the  periphery,  and  is,  therefore,  a 
result  of  vital  action,  (Compare  Figs.  311  and  321  with  Figs.  319 
and  320.) 


Miller. 


"  Micro-organisms  of  the  Hunian  Mouth. 


PATHOLOGY  AND  MORBID  ANATOMY. 


311 


3.  The  tubules  have  their  himen  lessened  in  diameter  in  the  trans- 
parent areas,  an  agreement  with  the  position  of  Walkhoff. 

4.  Secondary  dentine  may  accompany  the  process  in  contiguity 
with  the  area ;  moreover,  secondary  dentine  is  translucent.  It  indicates 
a  constructive  excitation  of  the  odontoblasts  of  which  the  dentinal 
fibrils  are  prolongations  (Fig.  311,  Sd). 

5.  Chemical  analysis  proved  that  no  lime  salts  had  been  lost,  and 
it  was  pointed  out  that  a  gain  in  the  percentage  of  salts  was  unnecessary, 


Fig.  320. 


Secondary  caries  of  dentine  advancing  from  pulp  chamber  and  therefore  occurring  after  death 
of  the  pulp.      Absence  of  transparency.      X  15.      (Miller.) 

as  new  dentine  is  necessarily  composed  of  organic  as  well  as  inorganic 
matter,  wherefore  the  analysis  would  not  necessarily  vary  from  that 
of  normal  dentine. 

6.  It  is  found  in  connection  with  abrasion  of  human  teeth  in  which 
the  activity  of  acid  may  possibly  be  an  open  question,  and  it  also 
occurs  in  the  worn  teeth  of  dogs,  the  saliva  of  which  is  strongly  alkaline. 

Miller  states  that  opacity  may  follow  or  be  associated  with  trans- 
parency.^ 

The  natural  conclusion  is  that  the  transparency  is  a  form  of  tubular 

1  Dental  Cosmos,  April,  1903. 


312 


DEXTAL  CARIES. 


calcification,  and  that  it  iinpedes  the  progress  of  caries;  that  it  does 
not  succeed,  as  a  rule,  is  due  to  the  overwhehning  action  of  the  bacteria. 

In  cavities  from  which  the  walls  are  broken  away,  freely  exposing 
the  carious  dentine  to  mastication,  the  carious  dentine  and  its  con- 
tained bacteria  may  be  removed  by  friction  (Fig.  329). 

In  the  transparent  area  the  tuljules  become  obliterated;  a  polished, 
discolored  surface  results  resembling  in  degree  an  abraded  surface. 
This  process  is  called  "eburnation"  and  is  really  tubular  calcification 
(which  see).     In  the  same  tooth  a  more  sheltered  border  of  this  spot 


Fir..   321. 


Transparency  resulting  from  cracks  in  the  enamel  at  a  and  b. 


20.      (Miller.) 


may  be  undergoing  the  carious  process.  Miller  records  cases  of  badly 
decayed  teeth  in  which  the  process  ceased  spontaneously  and  the 
dentine  became  hard  and  smooth. 

Pigmentation  in  Caries.  Pigmentation  occurs  in  caries  possibly  from 
extraneous  substances  entering  the  carious  area,  possibly  from  the 
substances  formed  during  putrefaction. 

The  slower  the  progress  of  the  decay  the  greater  the  discoloration. 
The  colors  vary  from  light  yellow  to  reddish-brown,  dark  brown, 
and  black. 

The  color  is,  as  a  rule,  darkest  upon  the  outside  of  the  carious 


PATHOLOGY  AND  MORBID  ANATOMY.  313 

dentine,  but  the  pigment  may  extend  through  large  masses  and  be 
found  staining  dentine  beneath  the  caries  hard  enough  to  leave 
in  situ.    As  a  rule  this  is  not  the  case. 

Black  suggests  the  possible  formation  of  sulphides.  Miller  has 
found  iron  almost  constantly  present  in  carious  dentine.  The  dis- 
coloration of  dentine  does  not  seem  to  be  necessarily  due  to  the  carious 
process,  as  it  may  be  seen  in  areas  of  abrasion.  In  a  specimen  pos- 
sessed by  the  editor  a  limited  cervical  caries  caused  a  growth  of 
secondary  dentine  and  an  area  of  tubular  calcification.  From  the 
pulpal  surface  of  the  secondary  dentine  to  the  area  of  caries  extends 
a  sharply  defined  area  which  has  a  flesh-rose  color  (Fig.  322).  Many 
areas  of  secondary  dentine  due  to  abrasion  are  stained  a  dark  brown. 

Artificial  caries  produced  in  teeth  placed  in  a  mixture  of  bread 
and  saliva  and  the  mixture  constantly  renewed  was  white.  If  putre- 
faction was  allowed  to  occur,  discolorations  ensued  (Miller). 

Fig.  322.  Fig.  323. 


CerAdcal   caries  associated   with    secondary  Caries  of  cementum  and  dentine  com- 

dentine.     Area  pigmented.  pletely  encircling  the  tooth. 

The  discolorations  of  carious  dentine  may  be  due  to  the  action  of 
chromogenic  bacteria.  Miller  isolated  from  the  mouth  an  organism 
which  he  named  bacillus  fuscans,  and  "which,  cultivated  on  the 
surface  of  nutritive  agar-agar,  in  a  few  weeks  imparts  to  the  medium 
a  yellowish-brown  color,  which  gradually  darkens  and  extends  deeper 
into  the  substratum  as  the  age  of  the  culture  increases." 

It  is  significant  that  the  three  acid-forming  organisms  found  by 
Goadby  in  the  deep  layers  of  carious  dentine  do  not  form  pigment 
in  their  artificial  media.     (See  p.  308.) 

Caries  of  Cementum.  Caries  of  cementum  occurs  when  the  gum 
has  receded,  exposing  the  cementum  to  the  fluids  of  the  mouth.  As 
a  rule  a  triangular  depression  exists  bounded  by  the  thickened  gum 
margin,  the  cementum,  and  the  enamel.  This  favors  the  collection 
of  the  bacterial  plaques  and  caries  follows.    The  gum  may  be  much 


314  DENTAL  CARIES. 

receded,  yet  no  caries  occur.  As  a  rule,  however,  recession  and  un- 
cleanliness  frequently  assure  its  presence.  Especially  is  this  true 
in  cases  of  general  recession  in  aged  or  debilitated  persons. 

The  path  of  bacterial  invasion  after  decalcification  is  by  way  of 
Sharpey's  fibres  to  the  lacunar  and  canaliculi;  later  the  dentine  is 
invaded  as  in  the  crown.  Frequently  the  form  of  the  cementum  is 
largely  retained  while  the  decalcification  is  deep  (Figs  322  and  323). 

CLINICAL  HISTORY  OF  CARIES. 

The  clinical  history  of  dental  caries  records  the  observable  phenom- 
ena associated  with  its  inception,  progress,  and  termination. 

Inception  of  Caries.  Caries  begins,  after  the  manner  described  in 
the  pathology,  at  favoring  spots.  As  a  rule  the  occlusal  fissures  of 
the  molar  teeth  are  first  decayed,  the  first  molars  being  often  carious 
in  this  situation  before  fully  erupted.  Uninformed  parents  usually 
consider  this  tooth  a  temporary  one  and  frequently  neglect  it.  It, 
moreover,  has  often  seriously  defective  fissures  which  afford  lodgement 
for  gelatinous  plaques,  which  seem  to  be  readily  formed  because  of 
the  unhygienic  state  of  the  temporary  teeth,  which  are  frequently 
carious.  Not  infrequently  a  cavity  is  produced  on  the  mesal  surface 
of  this  tooth  by  a  carious  condition  of  the  distal  surface  of  the  second 
temporary  molar.  In  other  mouths  both  teeth  are  affected  alike,  owing 
to  the  nature  of  the  approximation.  The  relative  liability  of  the 
various  surfaces  of  the  different  teeth  to  caries  may  be  averaged  for 
a  great  number  of  persons,  but  tables  drawn  from  clinical  cases  may 
have  little  application  to  one  particular  individual,  as  peculiarities  of 
local  predisposing  causes  and  personal  habits  modify  the  inception. 
Nevertheless  such  tables  are  exceedingly  interesting  as  showing  a 
general  relative  liability. 

Charts  have  been  made  by  Black  which  explain  themselves  (Figs. 
324  to  327).  The  figures  given  for  the  buccal  surfaces  of  the  third 
molars  seem  rather  lower  than  those  I  would  feel  w^arranted  in  giving  j 
certainly  after  adult  age  caries  frequently  occurs. 

The  lower  anterior  teeth  are  the  last  of  all  to  be  affected,  and  it  is 
common  to  see  the  six  lower  anterior  teeth  free  from  caries  years  after 
all  of  the  other  teeth  have  been  lost.  This  is  attributable  to  the  constant 
motion  of  the  saliva,  the  presence  of  calculus,  and  to  the  mechanical 
effects  of  tongue  movement,  lip  movement,  and  mastication. 

In  the  temporary  set  the  molars  decay  much  more  frequently  than 


CLINICAL  HISTORY  OF  CARIES. 


315 


Fig.  324. 


(- 

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Description  of  Charts. 
These  charts  represent  the  number  of  carious  cavities  observed  in  one  hundred  persons,  and  the 
position  of  these  cavities  on  the  individual  surfaces  of  the  teeth.  There  are  five  columns  of 
squares  devoted  to  each  tooth  of  one  side  of  the  mouth,  representins;  the  five  surfaces  as  shcmi 
on  the  left  hand.  The  number  of  cavities  in  the  surface  represented  is  shown  by  the  number 
of  squares  darkened,  so  that  the  effect  of  the  diagram  as  a  whole  gives  a  striking  picture  of  the 
frequency  of  decay  in  the  individual  surfaces  of  the  several  teeth.  On  the  right  the  percentage, 
or  the  number  per  hundred  persons,  is  given  in  figures  calculated  to  the  first  decimal  point. 
On  the  left  the  percentage  of  cavities  in  the  individual  teeth  for  all  surfaces  is  given  in  the  same 


316 


DENTAL  CARIES. 


■■(h. 


o 

r  I 

2  o 


I 


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-N 

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-N 

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■N 

MESIAL 

BUCCAL 

GRINDING 

LINGUAL 

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MESIAL 

BUCCAL 

GRINDING 

LINGUAL 

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mesial 
buccal 
grinding 

LINGUAL 
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MESIAL 

BUCCAL 

GRINDING 

LINGUAL 

DISTAL 

1    '    ! 

MESIAL 

BUCCAL 

INCISIVE 

LINGUAL 

DISTAL 

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incisive 

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^JGJppo^J^)pop;^) 


way.  The  cavities  occurring  on  one  side  of  the  mouth  only  are  represented.  And  only  one 
decay  in  an  indi^ndual  surface  is  counted;  that  is,  if  two  or  more  pits  are  found  decayed  in  the 
grinding  surface  of  a  molar,  but  one  is  counted;  and  the  same  rule  is  followed  with  all  of  the 
surfaces. 

Charts  Nos.  1  and  2  (upper  and  lower  jaw)  are  made  up  from  my  records  of  fiUings  for  628 
persons  of  all  ages,  and  therefore  represent  what  is  seen  in  practice  rather  than  the  actual  number 
that  may  occur. 

Charts  Nos.  3  and  4  (upper  and  lower  jaw)  are  made  from  100  of  my  own  patients  between  the 
ages  of  ten  and  twenty-five  years,  for  whom  I  have  filled  all  cavities  and  know  the  condition 
at  present.  They  represent  the  actual  number  of  cases  in  which  the  individual  surfaces  have 
decayed  in  these  100  persons.     (Black.) 


CLINICAL  HISTORY  OF  CARIES. 


317 


Fig.  326. 


c  X 

If 

a 


,e 


/c, 


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RD. 
OLAR 

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2nd. 
Molar 

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bbO,CbO,bC,CbsibW<j,b6bbCf,C    bbC/ibO>C>bbbCibbCriCr,CC,b>^<Jic 


the  incisor  teeth,  partly  because  longer  retained  and  partly  because 
of  the  width  of  their  approximations.  The  pulp  is  readily  exposed 
because  of  its  relatively  larger  size. 

Proximal  cavities  in  the  anterior  teeth  are  frequently  more  broad 
than  deep  and  present  problems  of  anchorage. 


318 


DEXTAL  CARIES. 


-ii 


o 

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•^    -J 

«-  Z 


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LINGUAL 

DISTAL 

MESIAL 

BUCCAL 

GRINDING 

LINGUAL 

DISTAL 

MESIAL 

BUCCAL 

GRINDING 

LINGUAL 

DISTAL 

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BUCCAL 
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v.  ,  z 

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Rapidity  of  Progress.  The  rapidity  of  progress  of  caries  depends 
upon  the  intensity  of  the  action  of  the  exciting  cause,  the  structure  of 
the  tooth,  and  the  nature  of  the  vital  resistance  offered.  The  exciting 
cause  will  act  most  intensely  in  mouths  ill  cared  for  and  containing 
much  carbohydrate  debris,  and  these  conditions  being  equal  enamel 


CLINICAL  HISTORY  OF  CARIES. 


319 


of  poorer  organization  and  presenting  a  greater  degree  of  solubility, 
in  teeth  presenting  broad  approximations,  will  be  the  more  rapidly 
destroyed. 

Williams  has  expressed  the  opinion  that,  as  a  rule,  the  process  of 
enamel  destruction  occupies  a  considerable  period  of  time,  a  fact 
which  may  account  for  the  general  lack  of  caries  in  the  temporary 
teeth  until  about  four  or  five  years  of  age.  The  decalcified  enamel 
may  retain  its  form  for  a  time  after  dentine  decalcification  has  begun. 

Fig.  328. 


*^..>.i^5 


Caries  undermining  enamel :  a,  masses  of  bacteria  lining  the  cavity.     X  50.      (Miller.) 


An  opaque  spot,  often  discolored,  is  seen  upon  the  tooth  and  is  readily 
broken  down  by  an  instrument  before  dentine  decalcification  occurs. 
If  the  approximating  tooth  be  extracted  the  carious  process  may  cease, 
owing  to  the  removal  of  the  bacterial  plaque  or  a  lack  of  food  supply 
(retention).  This  result  may  not  follow  if  the  dentine  has  been  invaded 
before  the  extraction. 

After  enamel  destruction  at  a  limited  area  caries  progresses  along 
its  inner  side  and  penetrates  the  dentine.    The  enamel  is  undermined. 


320  DEXTAL  CARIES. 

The  extent  of  cavity  orifice  is  no  certain  guide  as  to  the  depth  of 
penetration. 

Cases  are  frequently  observed  in  which  the  only  external  evidence 
of  caries  in  a  molar  or  bicuspid  is  a  white  or  bluish-black  line  marking 
the  fissure,  and  yet  the  dentine  may  be  deeply  and  widely  penetrated 
(Fig.  329,^). 

As  a  rule,  however,  as  the  cavity  in  the  dentine  enlarges  the  enamel 
at  the  orifice  becomes  disintegrated  so  that  the  orifice  is  enlarged  and 
more  food  debris  enters  to  accelerate  the  process  (Fig.  328).  A  deep 
cavity  may  thus  be  formed  before  the  patient  is  objectively  or  even 
subjectively  aware  of  its  existence.  After  a  time  the  occlusal  enamel 
boundary  of  the  cavity  breaks  down  and  food  is  even  more  readily 
admitted. 

It  has  been  noted  that  if  the  enamel  break  away  in  such  a  manner 
as  to  expose  the  carious  dentine  to  the  friction  of  food  masses  which 
are  not  retained  and  to  the  access  of  saliva,  the  progress  of  the  caries  is 
delayed  and  in  some  cases  ceases  altogether.  The  process  of  eburnation 
is  set  up.  (See  Transparent  Zone  and  Tubular  Calcification).  The 
latter  phenomenon,  however,  is  rarely  observ- 

FiG.  329.  .  . 

A  able  except  in  teeth  of  a  high  grade  of  organi- 

zation (Fig.  329,  B). 

Caries  may  progress  rapidly  for  a  period, 
and  then  receive  a  check  to  its  progress.  Teeth 
previously  free  from  the  disease  may  suddenly 
fall  victims  to  its  rapid  and  widespread  progress. 
No  doubt,  in  many  of  these  cases  there  are 
removed  from  or  added  to  the  local  oral  conditions  constitutional 
influences  which  deter  or  favor  the  local  development  of  caries,  pro- 
ducing bacteria. 

The  dentine  of  pulpless  teeth  is  more  rapidly  invaded  after  enamel 
decalcification  than  that  of  vital  teeth,  owing  to  the  absence  of  ^dtal 
resistance.  This  condition  does  not  necessarily  apply  to  the  enamel 
of  pulpless  teeth. 

While  caries  appears  at  all  ages  from  childhood  to  old  age,  its 
ravages  are  most  pronounced  and  its  progress  most  rapid  during  the 
period  of  adolescence  and  early  maturity.  Its  effects  are  most  marked 
between  the  ages  of  eight  and  twenty-five  years.  As  a  rule,  a  denture 
which  remains  for  twenty-five  years  unaffected  by  caries  remains 
unaffected  or  but  slightly  affected  to  an  indefinite  age.  To  be  sure, 
this  implies  two  conditions :  first,  that  the  active  causes  of  caries  have 


CLINICAL  HISTORY  OF  CARIES.  321 

been  in  but  slight  evidence;  and,  secondly,  that  the  denture  is  of  the 
highest  order.  The  classes  of  denture  which  escape  are  perfectly 
formed  and  symmetrically  arranged  teeth,  in  the  mouths  of  patients 
who  lead  sanitary  lives,  who  masticate  vigorously,  and  who  escape 
other  diseases. 

Caries  beginning  at  the  junction  of  the  cementum  and  enamel  of 
the  teeth  has  a  somewhat  different  clinical  history  from  that  noted 
when  its  occurrence  is  in  other  situations.  Its  progress  is  subject  to 
great  variations.  In  any  of  the  catarrhal  conditions  or  atrophic  con- 
ditions of  the  gum  which  lay  bare  the  neck  cementum,  caries  usually 
occurs.  It  occurs  also  as  a  process  secondary  to  mechanical  abrasion 
and  erosion  of  the  teeth.  Teeth  affected  by  erosion,  however,  as  has 
been  pointed  out,  are  commonly  exempt  from  dental  caries. 

The  Terminations  of  Caries.  After  the  pulp  is  exposed  it  sooner 
or  later  becomes  inflamed  and  hypertrophies  or  dies.  In  the  latter 
case  putrefaction  results,  which  for  a  time  may  exert  a  restraining 
influence  upon  decay,  but  not  for  a  long  time. 

Masses  of  food  freely  enter  the  pulp  cavity  and  caries  proceeds  in 
the  dentine  from  within  toward  the  periphery.  This  is  "secondary 
caries"  of  dentine,  and,  occurring  in  dentine  without  vitality,  no  trans- 
parency results  (Fig.  320) .  Notwithstanding,  caries  at  this  stage  proceeds 
rather  slowly,  particularly  if  the  crown  be  much  broken  down.  The 
result  of  secondary  caries  is  a  hollowing  out  of  the  dentine  of  the  root, 
and  finally  a  decalcification  of  the  cementum  which  may  persist  for 
some  time  as  a  thin,  elastic  wall.  Finally  this  is  destroyed  either  at 
the  occlusal  periphery  or  caries  causes  penetration  to  the  pericemental 
tissue.  This  may  occur  laterally  or  through  to  the  bifurcation  of  the 
roots.  In  either  case  it  is  called  "perforation  by  caries."  Into  this 
perforation  the  pericemental  tissue  may  become  protruded  by  hyper- 
trophy and  the  condition  of  fungous  gum  be  established.  Following 
the  breaking  down  of  the  crown,  the  blood  pressure  in  the  pericementum 
begins  an  extrusive  process,  the  pericementum  becomes  thickened,  and 
the  tooth  is  somewhat  loosened. 

Decay  of  the  root  face  and  breakage  of  the  cemental  margins  pro- 
ceed simultaneously  with  the  extrusion  until  finally  but  a  small 
discolored  bit  of  the  root  end  lies  upon  the  surface  of  the  gum,  from 
which  it  is  removed  by  some  slight  force  or  is  extracted. 

The  entire  process  of  caries  in  a  tooth  may  thus  extend  over  a 
period  of  from  ten  to  twenty  years. 

At  times  the  extrusive  force  pushes  a  root  up  sidewise,  particularly 

21 


322  DENTAL  CARIES. 

when  the  tooth  has  been  tipped  over  before  the  loss  of  the  crown. 
It  may  thus  be  retained  in  position  and  attached  upon  its  under  side 
for  some  time.  The  upper  side  may  be  pohshed  by  abrasion.  The 
exposed  end  of  a  root  undergoing  extrusion  is  also  sometimes  made 
smooth  by  abrasion.  A  bit  of  root  left  in  situ  after  breakage  during 
extraction  usually  undergoes  the  same  process  of  extrusion,  but  may 
not  decay  until  it  comes  under  oral  influences.  Usually  a  fistula  leads 
to  such  a  root,  but  very  rarely  the  gum  may  heal  over  it. 

Such  a  root  may  at  any  time  become  the  source  of  apical  abscess 
or  of  an  intractable  neuralgia. 


CHAPTER   XIV. 

DENTAL  CARIES:  DIAGNOSIS,  SYMPTOMS,  AND  PROGNOSIS. 

HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS. 

Diagnosis  of  Dental  Caries. 

The  diagnosis  of  dental  caries  is  made  through  both  objective  and 
subjective  symptoms.  The  signs  are  the  existence  of  cavities  and 
of  softened  areas,  directly  visible  or  made  evident  through  instru- 
mental means.  The  symptoms  are  pains  of  several  degrees  of  in- 
tensity. The  nature  and  intensity  of  the  pains  furnish  a  guide  to  the 
depth  of  the  carious  invasion,  and  but  an  indirect  indication  of  the 
location  of  the  disease. 

Diagnosis  by  Objective  Symptoms.  The  presence  of  the  markings 
of  superficial  decay,  decalcified  surfaces,  or  cavities  may  often  be  de- 
tected at  a  glance  or  be  seen  reflected  in  a  mouth  mirror.  Opacity  of 
enamel  is  usually  due  to  its  superficial  decalcification  or  caries  beneath 
it,  though  at  times  a  malformation  may  exist.  The  discoloration  or 
opacity  about  a  fissure  should  excite  suspicion  of  caries.  In  the 
routine  examination  for  cavities,  sharp,  finely  pointed  explorers  bent 
at  various  angles  are  to  be  passed  over  all  the  surfaces  of  the  teeth. 
If  the  enamel  at  any  point  admit  the  point  of  the  explorer,  caries  is 
usually  present.  Fissures  are  sometimes  deceptive  in  this  respect. 
A  good  rule  is  to  adjudge  the  presence  of  caries  when  the  point  catches 
slightly  as  removed. 

In  the  search  for  proximal  caries  great  care  is  required,  explorers 
with  very  short  points  being  often  necessary.  Frequently  a  cavity  may 
only  be  discoverable  from  one  point  of  access.  In  the  absence  of 
evident  cavities,  some  force  should  be  applied  to  detect  softened  spots 
of  enamel. 

Unwaxed  floss  silk  passed  over  carious  surfaces  indicates  a  rough 
surface  by  fraying.  It  may,  however,  at  times  pass  readily  over 
a  cavity  easily  detected  by  instruments;  so  that  it  is  not  absolutely 
reliable  as  a  test. 

The  strong  light  of  an  electric  mouth  lamp  transmitted  through  the 
teeth  exhibits  a  cavity  as  an  opaque  spot  outlined  upon  a  pinkish 


324 


Fig.  330. 


DENTAL  CARIES. 

Fig.  331. 


Dow  electric  lamp  for  mouth  illumination  with  re- 
flectors. Reflector  A  is  jointed  to  vary  the  angle  of 
reflection.  Reflector  B  is  for  illumination  of  the 
fauces.  Reflector  C  is  for  lateral  illumination.  (Jack.-) 

background.  It  not  only  permits  an 
easy  diagnosis,  but  also  affords  evi- 
dence of  the  depth  of  penetration.  ]\Ie- 
chanical  separators  or  wedges  are  at 
times  necessary  to  press  apart  con- 
tiguous teeth  sufficiently  to  admit 
^  exploring  instruments. 

The  necks  of  the  teeth  should  be 
examined  with  sharp  points  to  note 
any  softness  of  the  tooth  tissues.  The 
margins,  particularly  the  cervical  and 
neighboring  margins,  of  every  filling 
should  be  explored  to  test  the  integrity 
of  the  junction  of  filhng  and  tooth  or 
any  excess  or  deficiency  of  filling  ma- 
terial. 

The  examination  may  be  conducted 
by  one  of  two  systematic  methods. 
In  one  method  the  occlusal  faces  of 
all  the  teeth  are  first  examined  in  one 
survey,  then  the  interproximal  spaces, 
and,  lastly,  the  buccal  and  lingual  sur- 
faces of  the  teeth.  In  the  other  method 
every  portion  of  each  tooth  is  exam- 
ined, beginning  with  a  central  incisor 
or  terminal  molar,  before  passing  to 
the  adjoining  tooth. 

1  American  Text-book  of  Operative  Dentistry.  -  Ibid. 


Explorer  for  caries. 
(Jack.i) 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS      325 

Diagnosis  by  S abjective  Symptoms.  Complaints  by  patients  that 
salt,  sweet,  or  acid  substances  taken  into  the  mouth  cause  unlocalized 
or  partly  localized  pain  indicate  exposed  and  hypersensitive  dentine 
or  pulp  exposure.     Such  complaint  is  to  have  due  consideration. 

Pain  produced  upon  mastication  has  either  the  same  significance 
or  is  a  symptom  of  pericemental  irritation.  Apart  from  its  character 
as  a  symptom  of  caries,  hypersensitive  dentine  is  best  treated  of  as 
a  disease  of  the  dentine  consequent  upon  its  exposure  to  abnormal 
conditions. 

Prognosis  of  Caries. 

If  existing  caries  be  promptly  treated  in  youth  and  a  proper  system- 
atic prophylaxis  be  employed,  its  recurrence  during  youth  may  be 
largely  prevented.  At  about  adult  age  a  fair  degree  of  immunity  may 
be  expected.  In  the  absence  of  treatment  or  prophylaxis  the  exciting 
causes  seem  to  become  very  active,  and  many  teeth  may  be  lost  from 
caries  or  by  reason  of  extraction  for  pulp  and  pericemental  diseases. 
Extraction  itself  brings  many  evils  in  its  train. 

Even  advanced  caries  may  be  checked  by  proper  filling,  and  if  then 
prophylaxis  receive  due  attention  the  prognosis  for  the  teeth  is  gener- 
ally good;  indeed,  it  seems  as  though  but  few  conditions  exist  dependent 
upon  caries  alone  which  are  not  subject  to  correction  by  some  of  the 
means  within  the  resources  of  the  profession. 

Hypersensitivity  of  Dentine. 

The  exposure  of  dentine  to  external  agencies  is  so  commonly  followed 
by  an  increase  in  sensitivity  that  the  condition  requires  description 
in  itself.  It  is  a  general  condition  attendant  upon  abrasion,  erosion, 
and  caries,  and  has  a  therapeutics  of  its  own. 

The  term  sensitive  dentine  applied  to  this  condition  is  a  misnomer; 
all  vital  dentine  is  sensitive,  and  its  degree  of  sensitivity  differs  markedly 
in  individuals;  it  is  only  when  hypersensitivity  is  observed  that  the 
condition  becomes  pathological. 

Hypersensitivity  of  dentine  may  be  defined  as  such  a  degree  of 
sensitiveness  of  the  dentinal  fibrillse  as  interferes  with  the  comfortable 
excavation  and  shaping  of  a  cavity  of  decay ;  or  which,  in  the  absence 
of  dental  ministrations,  causes  painful  symptoms,  as  a  rule  reflected 
about  neighboring  parts. 

Causes  and  Pathology.  Normally  the  dentine  is  protected  from 
external  agencies  by  the  enamel  and  in  the  early  stages  of  gum  recession 
by  the  cementum. 


326  DENTAL  CARIES. 

With  the  removal  of  these  by  caries,  erosion,  abrasion,  or  fracture, 
the  terminal  filaments  of  the  dentinal  fibrillae  become  subjected  to 
sudden  variations  of  temperatures  ranging  from  a  little  above  32°  F., 
the  temperature  of  ice-water,  to  130°  F.,  that  of  very  hot  foods  or 
liquids. 

These  thermal  stimuli  at  times  give  evidence  of  their  effect  by 
producing  painful  sensations.  The  pulp  is  stimulated  through  the 
odontoblasts  and  their  relations  with  the  terminals  of  sensory  nerves 
in  the  pulp,  and  a  degree  of  vascular  overfulness  occurs  which  may 
be  denominated  mild  hyperemia.  The  effect  of  these  reactions  is  to 
cause  the  sensory  functions  of  the  pulp  to  become  somewhat  exalted, 
and  it  therefore  becomes  more  responsive  to  the  stimuli. 

Apart  from  the  effect  of  thermal  changes,  other  substances  act  as 
irritants.  The  lactic  acid  and  other  bacterial  products  in  the  cavity 
of  decay  without  doubt  play  a  part  in  exalting  the  irritability  of  the 
fibrillse.  Salt,  sweet,  or  acid  substances  introduced  into  the  mouth 
are  also  evidently  irritant,  as  active  symptoms  follow  their  application 
to  hypersensitive  dentine. 

Mechanical  abrasion  or  erosion  may  irritate  the  fibrillse,  or  at  least 
expose  them  to  the  action  of  other  irritants.  As  a  rule,  however,  the 
abraded  or  eroded  surfaces  are  protected  from  hypersensitivity  by  the 
process  of  eburnation.     (See  Transparent  Zone). 

The  scraping  of  necks  of  teeth  with  scalers  sometimes  induces  ex- 
posure of  dentine.  Within  cavities  of  decay  the  hypersensitivity  is 
greatest,  as  a  rule,  at  the  dentinal  periphery.  That  at  this  point 
the  dichotomous  endings  of  the  tubules  present  a  greater  number  of 
fibrils  to  the  action  of  the  irritant  is  quite  evident. 

In  cervical  hypersensitivity  the  cementum  or  enamel  is  removed  by 
abrasion,  erosion,  or  caries,  and  the  fibrillse  are  exposed.  The  presence 
of  the  granular  layer  of  Tomes  in  this  situation,  and  the  possibility 
of  this  layer  containing  the  expansions  of  the  fibrillse,  are  to  be  con- 
sidered. 

In  certain  cases  the  irritation  excited  by  the  touch  of  an  instrument 
to  dentine  adjacent  to  enamel  is  carried  to  the  pulp  by  anastomosing 
dentinal  fibrillse.  This  was  proven  by  a  few  cases  of  which  the  follow- 
ing is  an  extreme  one: 

In  a  central  incisor  secondary  dentine  had  filled  a  portion  of  the 
pulp  cavity  (Fig.  332,  SD).  Caries  had  subsequently  removed  the  incisal 
portion  of  this  secondary  growth  and  also  the  dentine-containing 
fibrils  leading  from  the  pulp  cavity  to  the  middle  of  the  incisal  edge. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS.     327 

The  application  of  an  excavator  to  dentine  in  the  incisal  portion  of 
the  cavity  (at  A),  the  fibrillse  of  which  could  have  no  direct  relation 
with  the  pulp,  produced  flashes  of  pain.  This  was  unmistakably  of 
the  character  of  hypersensitive  dentine. 

A  professional  friend  claimed  to  feel  sensitivity  in  a  cervicolingual 
cavity  of  a  molar  in  which  the  filaments  had  been  destroyed  by  suppu- 
ration for  one-third  of  the  length  of  the  canals. 
If  his  contention  was  true,  the  sensation  must 
have  been  conducted  by  way  of  the  granular 
layer  of  Tomes  to  the  level  of  the  pulp  and 
thence  by  the  fibrillse  to  its  substance. 

Spots  of  cervical  hypersensitivity  have  been 
occasionally  recorded  as  occurring  in  teeth  the 
canals  of  which  have  been  filled. 

Head^  records  a  case  in  w^hich  the  dentine 
bounding  the  pulp  canal  remained  hypersensi-        indirect   transmission  of 
tive  for  a  year  after  the  pulp  was  removed.    In     sensation  in  a  case  of  hj-per- 

•^     _  ...  sensitive  dentine:   li  1),  sec- 

this  connection  the  possibility  of  the  presence  ondary  dentine;  a,  point  of 
of  a  vital  pulp  filament  in  the  pulp  canal,  or  n^ic^)^"^^^^"^  ^'  ^^^^^ 
of  irritable  apical  tissue  receiving  the  impact 

of  liquid  forced  down  upon  it  by  a  canal  probe,  or  of  a  pericemen- 
tum irritable  to  touch  of  any  sort,  must  all  have  due  differentiation. 
I  have  never  seen  a  case  of  hypersensitivity  of  dentine  in  which  some 
filament  of  pulp  was  not  present  in  at  least  a  part  of  the  tooth. 

Dentine  cannot  become  inflamed,  as  leukocytes  cannot  enter  the 
tubules;  nevertheless  the  irritabihty  of  the  fibrillEe,  like  that  of  other 
protoplasm,  may  be  heightened.  It  has  been  noted  that  during  excava- 
tion of  a  cavity  the  irritability  is,  as  a  rule,  greatest  at  the  surface  of 
the  dentine — i.  e.,  at  the  point  at  which  irritants  are  present  in  greatest 
amount. 

With  hypersensitivity  other  functions  are  increased,  and  in  con- 
ditions producing  a  constant  stimulation  a  constructive  change  may 
occur  and  the  fibrillie  form  tubular  substance  at  their  own  expense. 
(See  Transparent  Zone  and  Tubular  Calcification). 

That  the  hypersensitivity  is,  as  a  rule,  a  disease  of  the  fibrils  involved 
or  of  the  fibrils  and  their  odontoblasts  is  shown  by  the  fact  that  occa- 
sionally of  two  cavities  in  the  same  tooth  one  will  present  a  hyper- 
sensitivity and  another  none;  again,  one  part  of  a  cavity  may  be 
hypersensitive  and  the  rest  not  so.     In  other  cases  perfectly  normal 

1  Dental  Cosmos,  1899. 


328  DENTAL  CARIES. 

dentine  is  hypersensitive,  as  noted  when  the  attempt  is  made  to 
reduce  a  sound  tooth  for  bridge  work. 

There  are  two  theories  accounting  for  the  transmission  of  the 
impulse  which  is  translated  by  the  patient  as  pain.  (1)  That  a  con- 
traction of  the  whole  cell,  fibril  and  odontoblast,  occurs,  the  sensory 
nerve  endings  being  pressed  upon  in  the  act.  (2)  That  a  wave-like 
motion  along  the  protoplasm  is  set  up,  causing  excitation  of  the  sensory 
nerves  and  due  to  the  incompressibility  of  the  water  (Gysi). 

The  former  is  analogous  to  the  contraction  of  a  voluntary  muscle 
cell  under  nerve  impulse.  The  whole  muscle  cell  contracts,  though 
the  nerve  ending  is  supplied  to  only  a  portion  of  it.^ 

This  hypothesis  fits  the  symptoms  as  excited  by  both  mechanical 
and  chemical  irritants,  while  the  latter  theory  does  not. 

Symptoms.  A  certain  degree  of  uneasiness  of  undefined  character 
may  at  times  be  noted  in  teeth  containing  cavities,  but,  as  a  rule,  pain 
other  than  pulp  pain  is  only  felt  upon  the  application  of  stimuli.  In 
some  cases  the  exposure  of  dentine  about  the  necks  of  teeth  may 
induce  such  an  unbearable  local  pain  or  neuralgic  condition  as  to 
positively  demand  relief. 

The  infiltration  of  acid,  salt,  or  sweet  substances  into  contact  with 
a  hypersensitive  surface  is  followed  by  a  wave  of  gnawing  pain  reflected 
usually  along  the  course  of  contiguous  nerve  filaments.  While  not 
definitely  localized  owing  to  the  fact  that  the  pulp  does  not  possess 
a  tactile  or  localizing  sense,  the  pain  may  usually  be  referred  to  a 
certain  part  of  the  mouth.  The  pressure  of  an  instrument  upon  the 
dentine  is  attended  by  a  flash  of  sharp  pain,  which  continues  for  a 
time;  but  lessens  if  the  contact  be  maintained.  In  this  test  the  pain 
is  localized  in  the  affected  tooth,  the  touch  of  the  instrument  being 
followed  by  a  recognition  of  position  by  the  tactile  organ  of  the  tooth, 
the  pericementum. 

Occasionally  food  forced  by  mastication  against  a  hypersensitive 
surface,  such  as  due  to  abrasion  or  caries  in  a  crevice,  will  produce 
a  sharp  pain  subsiding  promptly. 

Cavities  dried  for  filling  usually  produce  a  steady  pain,  caused  by 
dryness  and  relieved  by  an  analgesic  or  by  filling. 

It  is  beyond  doubt  that  individuals  differ  as  to  the  degrees  of  normal 
dentinal  sensitivity;  the  dentine  of  one  person  may  be  cut  freely  without 
evidence  of  marked  pain ;  in  another  the  touch  of  an  instrument  to  the 
newly  exposed  dentine  is  productive  of  a  parox}"sm  of  pain.     The 

'   Black,  American  System  of  Dentistry. 


HYPERSENSITIVE  DENTIXE  AND  ITS  THERAPEUTICS.      329 

difference  in  degree  of  irritability  is  manifested  in  another  manner: 
if  a  mild  sedative — for  example,  oil  of  cloves- — be  applied  to  the  hyper- 
sensitive dentine  of  one  person,  it  may  remove  the  distressing  symp- 
toms, but  with  others  it  may  be  necessary  to  employ  the  most  extreme 
measures  to  reduce  in  any  degree  the  hypersensitivity. 

The  general  perceptivity  of  the  individual  seems  to  play  a  part,  and 
even  apparently  normal  dentine  may  be  exquisitely  hypersensitive. 
Again,  pain  produced  in  excavating  may  be  due  to  the  character  of 
the  manipulation,  heavy  continued  burring  producing  heat;  lighter 
touches  may  excavate  equally  well,  but  produce  much  less  pain.  The 
dullness  of  the  excavator  or  bur  has  a  similar  effect. 

Diagnosis.  In  the  diagnosis  the  above  characteristic  symptoms  are 
to  be  considered.  The  decisive  test  is  made  by  pressing  an  instrument 
upon  the  suspected  surface,  when  the  characteristic  pain  is  produced, 
subsiding  upon  or  shortly  after  removal  of  the  contact. 

Upon  the  pulpal  wall  of  deep  cavities  doubt  may  exist  as  to  whether 
the  pain  is  due  to  pulp  irritation. 

A  suspected  exposure  may  be  differentiated  by  the  localization  of 
the  pain  upon  touch  to  a  point  corresponding  to  the  pulp  horn  or 
pulp  body,  or  by  the  point  catching  in  the  exposure.  Hyper- 
sensitive dentine  will  be  more  generally  distributed.  Pulp  abnor- 
mality or  approach  may  be  detected  by  means  of  a  drop  of  cool 
water  or  a  blast  of  cool  air  from  a  syringe.  (See  Hypersemia  of  the 
Pulp.) 

Treatment.  The  methods  of  treatment  which  have  been  followed 
for  the  relief  of  hypersensitivity  of  dentine,  and  the  induction  of  such  a 
degree  of  analgesia  as  will  permit  the  necessary  cutting  of  dentine, 
may  be  divided  into  general  and  local. 

General  Remedies.  The  general  remedies  employed  are  those 
which  abolish  or  lessen  the  perceptive  function  in  the  centres  of  the 
fifth  pair  of  nerves,  or  which  reduce  hyperirritability  of  the  nervous 
system.  Either  general  anaesthesia  or  general  anodynes  are  employed 
to  lessen  perception.  The  inhalation  of  a  few  whiffs  of  chloroform 
or  ethylic  ether  lessens  the  perception  of  pain.  Chloroform  is  avoided 
in  this  connection  on  account  of  its  dangers  when  used  in  the  sitting 
position.  Slight  etherization,  the  inhalation  being  carried  only  to  the 
benumbing  point,  affords  marked  relief  from  the  pain  incidental  to 
the  cutting  of  hypersensitive  dentine. 

The  administration  of  general  anodynes,  particularly  the  combina- 
tion of  morphia  and  atropia,  has  been  found  useful  in  this  field: 


330  DENTAL  CARIES. 

1^ — Morphinae  sulph.,  gr.  Va- 

AtropiniE  sulph.,  gr.  Viso- 

M.  et  ft.  pil.  No.  1. 
Sig. — To  be  taken  one-half  hour  before  operation. 

Flagg  noted  that  blondes  bear  morphine  sulphate  better  than 
brunettes;  particularly  are  nervobilious  and  bilionervous  patients 
idiosyncratically  opposed  to  its  use.  For  them  he  recommended  mor- 
phine bimeconate  solution  in  doses  equivalent  to  one-eighth  grain 
of  the  salt,  to  be  taken  one  the  evening  before  and  the  other  before 
the  operation. 

Chloral  in  five-grain  or  ten-grain  doses,  administered  in  water  before 
the  operation,  has  a  quieting  effect  upon  the  nervous  system.  Ambler^ 
has  suggested  the  use  of  from  ten  to  twenty  drops  of  fluid  extract  of 
piscidia  erythrina,  to  be  administered  about  ten  rninutes  before  oper- 
ating.    Drowsiness  may  be  expected. 

Hyoscyamine  hydrobromate,  ^^  grain,  will  be  useful  in  those  cases 
which  are  associated  with  muscular  spasm  or  hysteria. 

The  coal-tar  derivatives,  phenacetin,  acetanilid,  and  others,  are 
occasionally  efficient.  The  preparations  known  as  antikamnia  (said 
to  be  a  combination  of  acetanilid,  caffeine  citrate,  and  sodium  bicar- 
bonate) and  ammonol  (acetanilid  and  ammonium  carbonate,  equal 
parts)  are  to  be  preferred  in  this  connection.  The  dose  of  the  latter 
two  is  ten  grains,  administered  one-half  hour  before  operation. 

The  induction  of  the  hypnotic  state  belongs  in  the  category  of  means 
acting  upon  the  nerve  centres. 

Local  Treatment.  The  local  treatment  of  hypersensitive  dentine 
may  be  considered  from  two  standpoints,  according  to  whether  a 
concavity  containing  it  requires  excavation,  or  whether  the  hyper- 
sensitive spots  are  not  to  be  excavated  after  treatment. 

Treatment  in  Cavities  of  Decay.  The  remedies  employed  in 
the  endeavor  to  reduce  or  abolish  hypersensitivity  in  a  cavity  of  decay 
at  the  time  of  operation  are  quite  numerous;  few  are,  however,  always 
effective.    They  may  be  classed  under  two  headings: 

1.  Those  which  temporarily  benumb  or  anaesthetize  the  fibrillee  and 
prevent  the  transmission  of  sensation. 

2.  Those  which  chemically  destroy  the  fibrillse  for  a  distance,  thus 
preventing  transmission  of  sensation. 

Remedies  which  Benumb  the  Fibrille.  Chief  among  these  for 
its  universality  of  application  is  dryness.     Dentine,  which  protests 

1  Dental  Cosmos,  1901. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS.      331 

against  even  the  touch  of  an  instrument  while  wet,  has  its  sensitivity 
so  lessened  after  the  application  of  a  rubber-dam  and  drying  that  it 
may  be  cut  freely,  in  many  cases  without  the  aid  of  medicinal  agents. 
So  well  is  this  recognized  that  isolation  and  drying  of  teeth  are  regarded 
as  a  necessary  preliminary  to  cavity  preparation.  The  degree  of 
insensitivity  induced  is  in  proportion  to  the  dryness.  The  drying 
probably  deprives  the  dentinal  protoplasm  of  a  portion  of  its  water 
and  inhibits  the  transmission  of  sensation. 

A  continuous  blast  of  air  passed  from  a  compressed-air  apparatus 
through  a  heated  metal  bulb  and  nozzle  or  through  an  electrically 
heated  coil  should  be  employed  until  the  dentine  is  desiccated.  This 
is  evidenced  by  its  extreme  whiteness.  Other  forms  of  hot-air  syringes 
may  be  substituted  with  less  satisfaction. 

The  application  of  absolute  alcohol  assists  the  drying  because  of 
its  affinity  for  water.  Any  pain  produced  by  the  dryness  may  be 
relieved  by  the  application  of  a  mixture  of  equal  parts  of  carbolic 
acid  and  oil  of  cloves,  or  of  gum  camphor  and  carbolic  acid  (phenol- 
camphor),  both  of  which  have  some  angesthetic  effect. 

An  instrument  known  as  the  "dehydrator"  causes  absolute  alcohol 
placed  in  a  special  chamber  between  the  bulb  of  the  hot-air  syringe 
and  the  nozzle  to  be  vaporized  upon  the  hypersensitive  dentine. 
The  drying  effect  is  thereby  augmented  and  the  dentine  satisfactorily 
obtunded. 

Some  degree  of  dryness  is,  as  a  rule,  a  necessary  preliminary  to 
success  with  other  applications. 

Following  dryness,  the  excavation  should  be  done  with  sharp 
instruments  and  burs.  The  latter  should  only  be  lightly  touched  to 
the  dentine  and  be  revolved  at  high  speed.  Letting  the  bur  occasion- 
ally run  free  cools  it.  The  heat  of  friction  is  considerable  and  highly 
irritating. 

Refrigeration  by  a  spray  of  ether  or  ethyl  or  methyl  chloride  reduces 
the  temperature  of  the  fibrillse  and  pulp,  benumbing  them.  The 
rubber-dam  should  be  applied  to  isolate  the  teeth  operated  upon. 
Ether  is  applied  by  means  of  an  atomizer;  the  chlorides  are  contained 
in  glass  tubes  conveniently  capped.  The  cap  being  raised,  the  heat 
of  the  hand  causes  vaporization  of  the  agent  within  the  tube,  which 
forces  the  liquid  out  of  the  orifice  of  the  tube  in  a  fine  but  forcible 
stream.  The  cavity  should  at  first  contain  a  pellet  of  cotton  in  order 
that  the  dentine  may  be  gradually  obtunded  and  painful  response 
on  the  part  of  the  pulp  avoided. 


332  DENTAL  CARIES. 

"  Vapocain  "  and  "  potassocain,"  proprietary  agents  which  consist  of 
a  15  per  cent,  solution  of  cocaine  in  ether,  are  apphed  to  hypersensitive 
dentine  upon  the  theory  that  the  ether  enters  the  tubules,  carrying 
the  cocaine  into  contact  with  the  fibrillie;  the  ether  evaporates,  leav- 
ing the  cocaine  in  aqueous  solution  to  benumb  them.  This  requires 
several  minutes.  They  are  useful  in  the  deeper  cavities.  Jack  recom- 
mends that  the  cavity  acidity  be  neutralized  before  their  application.^ 

A  saturated  solution  of  cocaine  in  water  may  be  forced  into  the 
tubules  by  applying  it  on  a  pellet  of  amadou,  placing  over  this  soft 
vulcanite  rubber  and  producing  pressure  with  a  burnisher.  The 
pressure  should  be  gradually  applied.  A  gratifying  degree  of  dentinal 
anaesthesia  may  often  be  obtained. 

Adrenalin  chloride  solution  1  :  1000  plus  chloretone^  has  been  used 
in  this  manner  with  some  effect. 

A  crystal  of  cocaine  combined  with  an  equal  quantity  of  sodium 
chloride  may  be  placed  in  the  dried  cavity  and  wet  with  water.  After 
a  few  minutes  the  pain  of  cutting  will  be  lessened.  Some  pain  may 
occasionally  be  produced  at  first. 

Cataphoresis  (Greek  kata  down,  and  phoreo,  I  bear  or  bring)  is, 
in  technical  parlance,  the  transference  of  substances  from  the  anodal 
or  positive  pole  of  a  battery  toward  the  cathodal  or  negative  pole,  or 
in  some  cases  the  reverse. 

Cataphoresis  is  to  be  distinguished  from  electrolysis,  by  which 
substances  are  decomposed  and  their  elements  carried  from  positive 
to  negative  or  from  negative  to  positive  poles,  according  to  their 
polarity.  In  cataphoresis  a  substance  is  carried  unchanged  from  the 
positive  toward  the  negative  pole  after  the  manner  of  granules  in 
protoplasm  acted  upon  by  the  same  force.     (See  Chapter  I.) 

As  applied  to  dentistry,  a  primary  current  from  a  battery  arranged 
with  the  cells  in  series  has  the  positive  pole  or  conductor  connected 
with  a  resistance  or  current  controller  capable  of  being  so  manipulated 
as  to  gradually  reduce  the  resistance  to  the  current  a  fraction  of  a 
volt  at  a  time.  This  is  usually  a  broken  ring  of  graphite,  to  one  end 
of  which  the  incoming  current  is  admitted  by  means  of  the  conducting 
cord  and  travelling  indicator;  at  the  other  end  the  current  passes  out 
by  a  similar  cord,  which  in  turn  is  attached  to  a  milliamperemeter 
or  instrument  recording  the  quantity  of  current  passing  through  the 
circuit.  From  this  a  cord  leads  to  the  positive  electrode  applied  to 
the  tooth  cavity.     To  the  face,  neck,  or  wrist  of  the  patient  a  moist 

1  American  Text-book  of  Operative  Dentistry.  -  Parke,  Davis  &  Co. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS.      333 

electrode  (negative)  is  applied,  which  by  its  conducting  cord  leads 
the  current  back  to  the  negative  pole  of  the  battery. 

It  will  be  seen  that  the  current  passes  in  turn  from  the  positive 
pole  of  the  battery  to  the  resistance,  to  the  recording  instruments,  to 
the  patient  (another  resistance),  to  the  battery,  completing  the  circuit. 
These  are  said  to  be  arranged  in  series. 

In  the  use  of  the  cataphoric  apparatus  the  tooth  is  securely  insulated 
by  well-ligatured  rubber-dam  and  cotton  saturated  with  a  solution 
of  cocaine  hydrochlorate  or  citrate  of  a  strength  of  from  10  per  cent, 
to  a  saturated  solution  is  placed  in  the  cavity.  The  platinum  anode 
is  wrapped  with  cotton,  dipped  in  the  solution,  and  inserted  into 
contact  with  the  cotton  in  the  cavity.  The  controller  is  now  so  ma- 
nipulated as  to  gradually  cut  out  its  resistance  to  the  current  and  the 
high  resistance  of  the  dentine  is  gradually  overcome. 

The  cocaine  solution  should  be  renewed  as  dryness  occurs,  as  dryness 
increases  the  resistance.  The  cocaine  is  carried  along  the  fibrillse  to 
the  pulp  by  electric  osmosis,  and  dentinal  followed  by  pulpal  anaes- 
thesia results. 

From  eight  to  fifteen  minutes  or  sometimes  longer  are  required 
for  dentinal  anaesthesia,  which  loss  of  time  is  largely  regained  in  the 
facility  of  operation.^ 

Price^  has  shown  that  pulp  anaesthesia  is  gained  more  readily  by 
concentrating  the  action  of  the  cocaine  upon  the  pulpal  wall  by  means 
of  a  small  electrode.  If  general  dentinal  anaesthesia  is  required  he 
prefers  this  method,  as  the  pain  receptivity  of  the  pulp  is  abolished. 
A  broader  application  anaesthetizes  the  dentine. 

Woodward^  has  shown  that  in  the  latter  case  the  dentine  in  a  cavity 
upon  the  opposite  side  of  a  tooth  being  operated  upon  may  remain 
sensitive. 

The  pulp  may  be  anaesthetized  by  this  method  for  removal.  In 
diflScult  conditions  this  is  a  very  valuable  means  of  therapeutics. 

The  pulp  is  not  injuriously  affected  in  ordinary  applications,  but 
occasionally  a  hyperaemia  may  arise,  to  obviate  which  the  fibrillae 
should  be  treated  with  carbolic  acid. 

In  case  absolute  insensitivity  is  produced  the  anatomy  of  the  pulp 
must  carefully  be  considered,  so  that  it  be  not  exposed  during  the 
excavation  of  the  cavity.  Insulation  of  the  pulp  from  thermal  shock 
subsequent  to  filling  is  also  to  have  consideration. 

1  Jack,  American  Text-book  of  Operative  Dentistry. 

2  Dental  Summary,  April,  1903.  ^  International  Dental  Journal,  November,  1902. 


334  DENTAL  CARIES 

Soderberg^  has  shown  that  painless  excavation  of  cavities  otherwise 
uncontrolable  may  be  effected  by  the  use  of  nervocicHne,  an  alkaloid 
obtained  by  Dr.  D.  Dalma  from  the  East  Indian  plant  gasu-basu. 
Twenty-four  hours  are  required  for  complete  dentinal  ansesthesia 
without  pulp  anaesthesia  unless  a  second  application  be  made. 

The  primary  effect  of  nervocidine  being  irritating,  Soderberg  recom- 
mends the  additional  use  of  cocaine,  both  being  mixed  with  zinc  sul- 
phate cement. 

9; — Gum  arable,  3j. 

Zinc  sulphate,  Sss. 

Water,  fsj.— M. 
Dissolve  the  zinc  sulphate  in  the  water,  add  the  gum  arable,  stir;  let  stand  for  twenty-four 
hours,  strain. 

^ — Of  above  solution,  foij. 
Nervocidine,  gr.  x. 

Cocaine  hydrochlorate.  gr.  x. — M. 

To  a  portion  of  the  latter  solution  add  uncalcined  zinc  oxide  to 
make  a  cement,  which  is  placed  in  the  dried  cavity.  Uncalcined  zinc 
oxide  added  to  the  first  formula  makes  zinc  sulphate  cement.  After 
excavation  the  acidity  of  the  nervocidine  should  be  neutralized. 

Recently  hot  water  supplied  by  a  tube  leading  from  a  coil  heated 
by  electricity  and  attached  to  the  water  supply-pipe  of  the  fountain 
cuspidor  has  been  recommended  by  Dr.  A.  F.  Merriman,  Jr.,  for  the 
obtunding  of  hypersensitive  dentine  in  cases  in  which  dryness  is  not 
readily  obtainable,  nor  immediately  nor  subsequently  desirable. 

It  is  claimed  that  satisfactory  analgesia  is  obtained  and  that  the 
mucous  membrane  of  the  mouth  is  not  unduly  uncomfortable,  even 
when  the  heat  is  objectionable  to  the  finger  of  the  operator.  The 
advantages  of  the  method  for  excavation  and  grinding  are  obvious 
and  most  useful,  particularly  for  trimming  live  teeth. 

Remedies  which  Chemically  Destroy  Fibrill^e  for  a  Dis- 
tance, Preventing  Transmission  of  Sensation.  Agents  which 
chemically  destroy  the  dentinal  protoplasm  form  the  most  extensive 
group  of  dentinal  obtundents.  They  include  salts  of  metals,  such 
as  zinc  chloride  and  silver  nitrate;  carbolic  acid  and  its  derivatives 
and  like  bodies;  the  cresols,  etc.;  mineral  acids,  notably  sulphuric, 
chromic,  and  nitric;  organic  acids — trichloracetic  and  lactic  acids 
(full  strength);  alkalies — sodium  and  potassium  hydrates  and  car- 
bonates. 

Zinc  chloride,  silver  nitrate,  and  carbolic  acid,  all  cause  coagulation 
of  the  protoplasmic  processes  of  the  dentine.    The  mineral  and  organic 

1  Dental  Cosmos,  August,  1903. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS.       335 

acids  chemically  decompose  both  protoplasm  and  the  calcified  tissues. 
The  concentrated  alkalies  mentioned  chemically  destroy  protoplasm 
and  bring  about  its  quick  dissolution.  Like  all  active  chemical  sub- 
stances, the  extent  of  their  action  depends  upon  the  freedom  with 
which  they  are  applied. 

The  application  of  any  of  these  agents,  as  a  rule,  causes  pain,  the 
degree  of  suffering  being  usually  in  proportion  to  the  depth  of  the 
cavity.  For  this  reason  the  more  powerful  agents  like  zinc  chloride 
and  nitric  acid  are  to  be  confined  to  cavities  of  moderate  depth,  while 
carbolic  acid,  especially  in  combination  with  the  oil  of  cloves,  may  be 
used  in  the  deeper  ones. 

Fused  zinc  chloride  is  used  in  its  deliquesced  form  and  is  most 
active  when  some  of  the  salt  is  still  undissolved  in  the  bottle.  Its 
pain  in  suitable  cavities  is  a  full,  bearable  one,  gradually  increasing, 
sometimes  in  waves  until  a  crisis  is  reached,  when  the  pain  gradually 
ceases.  It  has  a  double  action,  not  only  coagulating  protoplasm,  but 
combining  with  its  water  owing  to  its  affinity  for  the  latter.  On 
account  of  this  property  its  action  may  be  limited  by  warm  water. 

An  undue  action  of  the  zinc  chloride  is  indicated  by  a  throbbing 
pain;  this  indicates  that  the  pulp  has  been  irritated.  When,  as  occa- 
sionally occurs,  no  pain  is  produced,  no  obtundent  effect  is  obtained. 
If  this  occur  often  the  drug  is  oversaturated  with  water. 

Bogue  has  suggested  that  cocaine  crystals  be  incorporated  with  the 
chloride  of  zinc  as  a  means  of  alleviating  the  pain  incident  to  the 
application. 

Certain  moderately  deep  cavities  may  be  filled  with  oxychloride  of 
zinc  cement,  the  free  zinc  chloride  acting  as  an  obtundent.  This 
requires  a  prolonged  action  and  is  only  resorted  to  in  cases  which  do 
not  admit  of  immediate  work,  or  in  which  procrastination  is  desirable. 

A  formula  of  wide  renown  is  known  as  Robinson's  remedy;  this 
may  be  made  in  one  of  two  ways: 

^fl- -Potassium  hydrate 
(or  Sodium  hydrate), 

Carbolic  acid,  da. — M. 

Reduce  the  gelatinous  mass  formed  with  alcohol. 


Or, 


^ — Sodium  hydrate  (deliquesced), 

Calvert's  crystal  carbolic  acid,  da. — M.      (Huey.) 

The  liquid  formed  is  spoiled  when  it  efHoresces  upon  the  sides  of  the  bottle  neck. 


The  painfully  caustic  action  of  the  sodium  or  potassium  hydrate 
is  modified  by  the  carbolic  acid. 


336  DENTAL  CARIES. 

The  application  is  useful  in  the  simpler  cavities  and  about  the 
undecayed  but  hypersensitive  necks  of  teeth. 

If  this  remedy  or  zinc  chloride  be  required  about  the  periphery  of 
deep  cavities  the  plan  suggested  by  Jack/  of  varnishing  the  cavity 
floor  with  chloro-percha  as  an  impenetrable  protective,  is  valuable. 

A  solution  of  gutta-percha  in  oil  of  eucalyptus  will  serve  equally 
well  for  the  purpose. 

The  combination  of  potassium  carbonate  with  glycerin  makes  a 
water-extracting  combination  having  but  little  coagulating  power. 
For  this  reason  it  may  be  used  in  the  deeper  cavities,  but  not  in  cases 
of  almost  exposed  pulp,  as  in  such  cases  its  application  is  painful. 

p. — Potassium  carbonate,  gr.  xv. 

Glycerin,  fSj. 

Mix  in  a  mortar. 
To  be  applied  on  a  pellet  of  cotton.     (Flagg.) 

It  may  be  used  with  effect  even  upon  slightly  moist  dentine. 

Not  being  escharotic  to  the  gum,  this  remedy  is  exceedingly  useful 
about  the  sensitive  but  undecayed  necks  of  teeth,  and  may  be  freely 
applied  after  moderate  drying  of  the  parts. 

If  necessary  the  patient  may  be  given  the  prescription  and  directed 
to  apply  by  means  of  a  clean  tooth-pick,  which  should  not  be  used 
a  second  time,  as  the  mixture  may  be  infected  and  spoiled. 

Its  pain  simulates  that  of  zinc  chloride,  but  is  less  severe  in  its  char- 
acter. 

A  mixture  of  tannin  and  glycerin  has  a  similar  effect. 

Jt — Tannin,  5j  or  5ij. 

Glycerin,  fSj. 

Mix  in  a  warm  mortar. 

Carbolic  acid  in  concentrated  form  may  be  applied  to  any  cavity. 
Jenkins,  of  Dresden,  has  recommended  that  it  be  used  hot;  it  is  par- 
ticularly useful  for  cavities  containing  masses  of  softened  dentine. 

Sodium  bicarbonate  is  at  times  an  efficacious  remedy  and  may  be 
freely  applied  to  the  moist  cavity. 

A  20  per  cent,  solution  of  ammonium  carbonate,  applied  for  five 
minutes  or  longer,  is  useful." 

The  nitrate  of  silver  powerfully  coagulates  fibrillar  protoplasm,  and 
is  useful  in  posterior  teeth  well  out  of  view  and  to  which  the  rubber- 
dam  cannot  well  be  applied.  It  is  also  useful  about  undecayed  hyper- 
sensitive necks  of  molar  teeth.    It  discolors  the  dentine,  metallic  silver 

1  American  Text -book  of  Operative  Dentistry. 

2  Thiesing,  Dental  Cosmos,  November,  1903. 


HYPERSENSITIVE  DENTINE  AND  ITS  THERAPEUTICS.      337 

being  deposited.  For  this  reason  its  use  is  ordinarily  confined  to  pos- 
terior teeth,  though  in  some  obstinate  cases  of  hypersensitive  necks  of 
lower  incisors  and  cuspids  it  may  be  used. 

The  subsequent  use  of  sodium  chloride  assists  in  partially  removing 
the  stains,  argentic  chloride  being  formed. 

Register  has  suggested  the  use  of  iodine  followed  by  ammonia  for 
this  purpose.  * 

In  shallow  cavities  and  upon  abraded  surfaces  nitric  and  chromic 
acid  accurately  applied  in  small  quantity  upon  a  gold  probe  is  useful. 
Any  softened  dentine  must  later  be  removed  and  filled. 

Aside  from  the  treatment  of  hypersensitive  dentine  at  the  time  of 
operation,  analgesics  may  be  introduced  for  their  power  of  gradually 
lessening  the  hyperirritability  of  fibrillar  protoplasm.  If  cotton  wedges 
are  introduced  antiseptic  analgesics,  particularly  oil  of  cloves  and 
phenol-camphor,  may  be  used  on  the  cotton  with  advantage. 

A  partially  prepared  cavity  may  be  moistened  with  oil  of  eucalyptus 
and  temporarily  filled  with  temporary  stopping  or  gutta-percha. 

A  temporary  filling  made  by  mixing  zinc  oxide  with  Fletcher's 
carbolized  resin  or  eugenol  to  a  stiff  paste  will  endure  a  week  or  more 
and  reduce  hypersensitivity. 

^ — Carbolic  acid, 

Colophony,  dd      Sj. 

Chloroform,  fsss. — M.     (Fletcher.) 

The  above  may  be  applied  on  cotton  for  a  day  or  two  with  advantage. 

In  cases  in  which  devitalization  is  intended,  arsenic  may  be  used 
as  an  obtundent  to  effect  a  deeper  placing  of  another  portion  as  a 
devitalizing  agent;  twenty-four  to  forty-eight  hours  are  required  for 
this  purpose.  If  left  long  enough  it  will  devitalize  the  pulp  even 
through  a  large  mass  of  dentine. 

There  is  no  safety  in  short  applications  as  a  means  of  obtunding 
dentinal  hypersensitivity.  The  pulp  may  die  even  after  seeming 
excavation  of  all  affected  dentine. 

Ninety  per  cent,  of  cavities  may  be  comfortably  excavated  with 
sharp  instruments  by  the  aid  of  dryness  and  carbolic  acid.  A  small 
percentage  require  the  use  of  caustics,  etc.,  while  in  a  still  smaller 
number  cataphoresis  is  the  only  certain  remedy. 

During  seasons  in  which  acid  fruits  are  consumed  much  h}^er- 
sensitivity  may  be  induced.  This  should  always  lead  to  examination 
for  cavities  of  decay,  but  such  may  not  exist  or  may  be  properly  filled. 

For  hypersensitivity  about  undecayed  necks  of  teeth,  the  mouth 

22 


338  DENTAL  CARIES. 

should  be  kept  in  an  alkaline  condition  by  means  of  dilute  phenol 
sodique  or  sodium  bicarbonate,  or,  better,  by  the  use  of  more  lasting 
mild  alkalies,  such  as  chalk,  or  milk  of  magnesia,  or  a  combination  of 
the  two. 

The  use  of  the  potassium  carbonate  in  glycerin  is  indicated  and 
may  be  given  to  the  patient  for  free  use. 

For  hypersensitive  incisal  edges  or  occlusal  surfaces  Robinson's 
remedy  may  be  dispensed. 

At  times  zinc  chloride,  Robinson's  remedy,  and  silver  nitrate  must 
be  used  by  the  operator.  In  very  obstinate  cases  of  cervical  hyper- 
sensitivity Flagg  has  recommended  the  use  of  the  electric  cautery, 
the  spots  to  be  seared. 

In  a  number  of  the  localized  cases  fillings  may  be  subsequently 
required  unless  rigid  prophylaxis  be  practised.  Acid  mouth  washes 
should  be  avoided. 


CHAPTER   XV. 

DENTAL  CARIES:    THERAPEUTICS  AND  PROPHYLAXIS. 

According  to  the  depth  of  invasion  and  variations  in  the  thera- 
peutics involved,  caries  may  be  divided  into  eight  stages  as  follows: 

1.  Superficial  caries,  or  that  stage  in  which  the  enamel  has  been 
partially  decalcified  but  the  dentine  not  affected. 

2.  Simple  caries,  in  which  the  dentine  has  been  affected  slightly 
in  such  a  manner  as  ordinarily  to  compel  the  formation  of  a  cavity 
and  its  filling. 

3.  Deep-seated  caries,  in  which  the  complete  excavation  of  the 
cavity  renders  pulp  injury  a  possibility,  but  the  pulp  is  not  very 
dangerously  approached. 

4.  Almost  exposed  pulp.  This  is  a  refinement  of  the  preceding 
stage,  in  which  pulp  exposure  becomes  an  imminent  danger  during 
excavation  of  the  cavity  and  special  therapeutics  are  demanded. 

5.  Exposed  pulp,  in  which  the  actual  exposure  of  the  pulp  by 
decay  or  by  accident  or  intention  during  excavation  renders  its  treat- 
ment necessary,  or  in  which  disease  of  the  pulp  compels  canal  treat- 
ment. 

6.  Perforation  by  caries,  in  which  after  pulp  death  secondary  caries 
of  dentine  and  cementum  has  caused  an  opening  into  the  pericemental 
tract. 

7.  Loss  of  crown  by  caries. 

8.  Loss  of  root  by  caries. 

Each  of  these  stages  of  caries  requires  special  consideration  and  a 
therapeutics  adapted  to  each. 

THERAPEUTICS  OF  SUPERFICIAL  CARIES. 

About  cavity  margins,  beneath  green  stain,  etc.,  and  at  points  of 
proximal  contact  of  teeth  may  frequently  be  seen  areas  of  enamel 
decalcification,  the  enamel  not  being  entirely  penetrated  (Fig.  296). 

It  is  possible  at  times  to  remove  the  decalcified  portion  by  means 
of  carborundum  strips,  files,  or  disks.  If  the  surface  be  highly 
polished    by  means  of   pumice  and  chalk  and  subsequent   prophy- 


340  DENTAL  CARIES. 

laxis  be  employed,  the  practice  may  be  endorsed  for  the  better  grades 
of  teeth,  and  particularly  in  the  anterior  part  of  the  mouth.  As  a 
rule,  however,  the  attempt  to  remove  supposed  superficial  enamel 
caries  demonstrates  the  fact  that  the  enamel  is  deeply  affected,  and  in 
all  probabiUty  the  dentine  as  well.  The  attempt  to  remove  such 
caries  upon  proximal  surfaces  by  files  and  stones  results  in  tooth 
deformity,  the  exposure  of  dentine  to  the  fluids  of  the  mouth,  and  the 
destruction  of  the  contact  points,  except,  perhaps,  when  in  the  anterior 
teeth  a  lingual  approach  is  made.  It  may  be  considered  a  safe  rule 
to  examine  by  means  of  the  electric  mouth  lamp  any  cases  of  suspected 
superficial  caries  in  order  to  determine  the  depth  of  enamel  invasion. 

The  large  majority  of  such  cases,  especially  in  the  poorer  grades 
of  teeth,  will  be  found  to  be  of  the  class  called  here  simple  caries. 

Upon  the  labial  or  buccal  surfaces  of  anterior  teeth  a  superficial 
decalcification  may  be  found.  This  may  be  removed  by  abrasives, 
the  surface  highly  poHshed,  and  the  patient  enjoined  to  use  great  care 
in  prophylaxis.  Any  spots  at  which  simple  caries  exists  should  be 
excavated  and  filled. 

A  superficial  caries  of  cementum  and  dentine  may  exist.  This  may 
be  removed,  the  dentine  pohshed,  and  nitrate  of  silver  applied  if  the 
surfaces  be  not  exposed  to  view. 

The  superficial  decay  about  cavity  margins  should  either  be  disked 
off  or  the  area  included  in  the  cavity,  if  disking  be  judged  capable  of 
inducing  recurrent  caries. 

THERAPEUTICS  OF  SIMPLE  CARIES. 

The  cases  cited  above  and  all  detectable  cavities  of  very  limited 
depth  may  be  classed  as  cases  of  simple  caries.  The  teeth  should  be 
wedged  apart  if  this  be  needed  for  access,  all  decalcified  enamel  and 
dentine  removed,  the  ca^dty  properly  extended  and  shaped,  and,  as 
a  rule,  a  filhng  of  gold  inserted.  All  fissures  about  a  ca\Tity  should  be 
freely  opened  to  their  extremities  and  made  a  part  of  the  general  cavity. 

At  times,  expediency — i.  e.,  the  systemic  condition  of  the  patient, 
the  character  of  the  decay  or  of  the  surrounding  tooth  structure  or 
economy — warrants  the  use  of  a  good  amalgam,  or  occasionally  of 
gutta-percha,  in  suitable  locations  not  exposed  to  attrition.  Upon 
the  labial  surfaces  of  incisors  porcelain  inlays  combine  efficiency 
with  aesthetics. 

If  a  simple  ca\dty  prove  inordinately  sensitive,  the  more  powerful 


THERAPEUTICS  OF  DEEP-SEATED  CAPJES.  341 

remedies  may  be  used  to  reduce  the  hypersensitivity,  and  the  ca\'ity 
should  be  treated  with  carboHc  acid  before  filling,  particularly  when 
gold  is  to  be  used  in  cervicolabial  cavities  of  incisors.  By  this  means 
the  subsequent  effect  of  thermal  changes  is  lessened. 

THERAPEUTICS  OF  DEEP-SEATED  CARIES. 

In  this  stage  of  caries  there  is  usually,  although  by  no  means  always, 
an  easily  discoverable  cavity  of  size.  After  the  removal  of  ragged  and 
overhanging  enamel  margins,  and  of  loose  debris  in  the  ca^dty,  it  is 
noted  that  the  response  to  thermal  impulse  is  painful  and  prompt.  In 
washing  such  cavities,  water  at  a  temperature  of  about  100°  F.  should 
always  be  used;  cold  or  very  hot  water  being  only  employed  in  cavity 
irrigation  to  test  the  promptitude  of  response  upon  the  part  of  the 
pulp. 

In  treating  hypersensitivity  of  dentine  the  mineral  acids  are  avoided, 
and  if  strong  agents  like  zinc  chloride  are  used,  the  cavity  floor  is  to 
be  varnished  with  chloro-percha  or  formo-percha,  which  are  imperme- 
able. If  necessary,  essential  oils  or  a  saturated  solution  of  cocaine  in 
glycerin,  thymol  in  alcohol,  or  menthol  in  chloroform  may  be  sealed 
in  for  twenty-four  hours. 

A  mixture  of  cocaine  with  nervocidine  may  be  useful,  as  indicated 
by  Soderberg. 

Cocaine  cataphoresis  is  regarded  as  admissible  in  all  stages  of  caries. 

The  removal  of  the  softened  dentine  in  these  cases  forms  a  ca^dty  of 
such  magnitude  that  proximity  to  the  pulp  is  e^ddent.  The  softening 
has  proceeded  for  a  distance  beneath  the  enamel,  so  that  when  all 
softened  dentine  is  cut  away  from  beneath  the  enamel  the  latter  tissue 
overhangs,  unsupported,  the  general  cavity.  These  overhanging  walls 
are  cut  away  until  the  region  of  normal  enamel  is  reached,  and  then  it 
may  be  that  the  walls  still  overhang  the  general  cavity.  It  is  usually 
not  necessary  nor  advisable  to  remove  this  portion  of  enamel. 

At  the  completion  of  excavation  the  pulpal  wall  of  the  ca^dty  T\ill 
be  in  close  proximity  to  the  pulp.  A  blast  of  cool  air  from  a  chip 
syringe  may  produce  an  immediate  response  upon  the  part  of  the 
pulp,  vigorous  in  proportion  to  the  thinness  of  its  dentinal  covering 
and  its  irritability. 

In  many  cases  non-conducting  substances  are  required  as  inter- 
mediates between  the  pulpal  wall  and  the  metal  filling.  In  many 
other  cases  the  metal  filling  may  be  placed  directly  upon  the  dentine 


342  DENTAL  CARIES. 

without  danger.  In  some  cases  a  simple  layer  of  non-conducting 
varnish,  such  as  "  cavitine, "  will  be  sufficient.  In  others  zinc  phosphate 
or  gutta-percha  must  be  added.  The  degree  of  the  response  to  a  blast 
of  cool  air  will  afford  a  guide  to  the  nature  of  the  intermediate  required 
if  any  be  deemed  necessary.  In  no  case  should  varnish  or  gutta-percha 
be  allowed  to  remain  in  the  portions  of  ca\dty  that  support  the  covering 
filling  material  and  which  is  subjected  to  the  force  of  mastication. 
The  resilient  nature  of  such  substances  will  cause  the  loosening  of 
the  filling. 

In  some  cases  the  undermined  state  of  the  enamel  walls  necessitates 
the  use  of  an  adhesive  zinc  phosphate  as  a  means  of  support  by  replac- 
ing the  lost  dentine,  and  in  such  the  pulpal  wall  may  be  covered  and 
so  protected  from  impact  as  well  as  from  thermal  changes. 

The  action  of  zinc  phosphate  upon  dentinal  fibrillae  and  the  pulp 
being  a  matter  of  some  doubt,  it  is  better  that  the  pulpal  wall  be 
varnished  before  it  is  introduced.  The  varnish  not  only  acts  as  an 
impervious  coating,  but  also  serves -^as  an  additional  non-conductor. 
If  made  antiseptic  it  is  still  more  useful. 

After  the  cavity  is  prepared  it  is  sterilized  and  dried  as  described 
in  the' next  stage  of  caries,  is  coated  with  "cavitine"  varnish,  and 
Harvard  zinc  phosphate  mixed  stiff  is  packed  into  the  undercuts  and 
over  the  pulpal  wall. 

A\hen  set  the  enamel  margins  are  freed  of  cement  and  the  cement 
is  excavated  to  the  form  required.-  In  some  cases  cement  can  only 
be  placed  over  the  pulpal  wall. 

In  deep-seated  caries  the  extension  of  cavity  margins  in  such  a 
manner  as  to  prevent  recurrence  of  decay  is  demanded.  Upon  prox- 
imal surfaces  the  ideal  conditions  are  an  extension  of  buccal  and 
lingual  margins  to  a  point  which  will  permit  a  contoured  metal  filling 
to  have  its  corresponding  buccal  and  lingual  margins  well  irrigated 
by  the  action  of  the  toothbrush  and  food  in  mastication. 

The  cervical  margin  of  the  cavity  and  filling  are  best  protected  when 
overlapped  by  healthy  gum  tissue,  and  if  possible  should  be  so  arranged. 
The  cervical  margin  should  always  be  extended  beyond  the  contact 
point  in  such  cases,  whether  carried  beneath  the  gum  or  not.  Incisal 
margins  are  to  have  similar  consideration. 

Firm  proximal  contact  of  fillings  or  filling  and  tooth  are  required 
to  prevent  packing  of  food  into  the  interproximal  space.  This  would 
both  injure  the  gum  and  introduce  the  fermentable  element  in  caries 
production.    The  point  of  contact  should  be  neatly  rounded  so  as  to 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP.  343 

cause  as  little  contact  as  possible.  This  contact  should  be  obtained 
even  if  the  filling  must  be  overcontoured  at  times. 

An  exception  may  at  times  be  made  where  a  space  has  previously 
naturally  existed  and  the  gum  margin  is  healthy. 

Teeth  should  never  be  joined  by  fillings  alone.  If  necessary  for 
the  protection  of  the  gum,  both  may  be  crowned  and  the  crowns  united 
by  solder,  or  a  staple  may  be  placed  in  the  pulp  canals  of  the  two 
teeth.  About  this  a  common  filling  may  be  built.  (See  Pyorrhoea 
Alveolaris.) 

THERAPEUTICS  OF  ALMOST  EXPOSED  PULP. 

In  this  stage  of  caries  complaint  is  usually  made  that  for  some 
time  pain  has  been  produced  by  the  presence  in  the  mouth  of  cool 
or  hot  substances.  Several  classes  of  almost  exposed  pulps  may  be 
discovered  after  opening  the  cavity  and  removing  the  bulk  of  the 
decayed  dentine.  In  the  simplest  class  the  pulpal  wall  may  be  found 
sound  after  removal  of  all  decalcified  dentine.  This  makes  practically 
a  case  of  deep-seated  caries  and  is  to  be  treated  as  such,  the  close 
approach  to  the  pulp  simply  demanding  additional  precautions  as 
to  non-conduction,  prevention  of  compression,  and  infection.  The 
cavity  is  to  be  sterilized  with  1  per  cent,  formaldehyde,  5  per  cent, 
sodium  dioxide  solution,  etc.,  and  dried;  over  the  pulpal  wall 
"cavitine"  with  hydronaphthol  added  is  painted  and  dried: 

P — Hydronaphthol,  gr.  ij. 

Alcohol,  gtt.  XX. — M. 

Add  to  the  half-ounce  bottle  of  "cavitine.''^ 

A  thin  wafer  of  softened  gutta-percha  is  to  be  laid  over  the  pulpal  wall 
in  such  manner  as  not  to  interfere  with  the  introduction  of  cement. 
Harvard  zinc  phosphate  mixed  to  a  consistency  just  suited  to  the  case 
may  be  pressed  laterally  into  the  undercuts  and  will  spread  nicely 
over  the  gutta-percha  without  pressure.  Under  no  circumstances 
must  the  superstructures  depend  upon  the  gutta-percha  base  as  a 
support,  as  the  filling  may  loosen  or  the  wall  be  broken. 

The  operation  may  be  varied  for  cases  of  but  limited  retaining 
periphery  by  gently  spreading  the  zinc  phosphate  over  the  varnish, 
or  in  some  cases  the  gold  and  zinc  phosphate  or  amalgam  and  zinc 
phosphate  combination  may  be  required. 

In  the  use  of  gold  and  zinc  phosphate  a  portion  of  crystal  gold  is 

^  "Cavitine,"  or  "crystalline"  of  commerce,  is  composed  of  trinitrocellulose  dissolved  in  sub- 
acetate  of  amyl. 


344  DENTAL  CARIES. 

gently  tapped  into  a  mass  of  soft  cement  placed  over  the  varnish  and 
the  setting  of  the  cement  awaited.  The  gold  is  then  condensed  and 
more  added. 

With  the  amalgam  and  zinc  phosphate  combination,  after  placing 
the  gutta-percha,  soft  cement  is  placed  upon  one  cavity  margin  and 
a  ball  of  previously  prepared  amalgam  is  laid  upon  it.  Pressure  upon 
the  amalgam  by  means  of  a  ball  burnisher  causes  the  cement  to  be 
spread  over  the  cavity  wall  in  advance  of  the  amalgam.  The  margins 
are  freed  of  amalgam  and  cement  and  the  operation  is  completed 
with  amalgam. 

This,  of  course,  refers  to  locations  in  which  the  latter  is  indicated. 
The  cement  in  the  combination  increases  the  adhesion  and  prevents 
leakage  and  the  discoloration  of  the  walls  by  the  amalgam.  A  trifle 
of  aristol  or  hydronaphthol  added  to  the  cement  (1  to  10)  imparts  to 
it  an  antiseptic  character  without  impairing  its  integrity  as  a  cement. 

The  second  class  of  almost  exposed  pulp  is  that  in  which  thorough 
excavation  would  cause  exposure  of  the  pulp. 

If  the  dentine  be  of  the  disintegrated,  boggy  sort,  it  should  be 
removed  regardless  of  exposure;  but  if  it  be  simply  softened  by 
decalcification  and  be  quite  firmly  adherent  to  the  cavity  floor,  and 
particularly  if  it  be  somewhat  thickly  distributed,  the  deeper  layers 
may  be  left  in  situ,  as  a  pulp  covering. 

In  such  cases  all  lateral  walls  should  be  thoroughly  excavated  and 
only  a  thin  layer  left  over  the  pulp  horns.  While,  without  doubt,  the 
tubules  of  decalcified  dentine  are  liable  to  be  invaded  by  bacteria, 
Miller  has  shown  that  frequently  such  dentine  may  exist  without 
invasion. 

The  argument  that  such  dentine  contains  poisonous  products  of 
bacteria  deleterious  to  the  pulp  does  not  seem  borne  out  by  results 
in  carefully  handled  cases. 

That  some  of  these  protected  pulps  may  die  is  a  fact  not  to  be 
disputed,  but  that  many  live  in  security  is  also  true.  Whether  such 
dentine  can  be  recalcified  has  not  yet  been  scientifically  shown,  but  cer- 
tain cases  treated  with  oxychloride  of  zinc  have  shown  evidences  of 
it,  and  Miller  records  cases  of  hardening  of  such  caries  even  without 
treatment. 

The  treatment  required  by  this  dentine  is  first  neutraHzation  of  the 
acid  present;  second,  saturation  with  a  permanent  antiseptic;  third, 
an  antiseptic  non-conductive  covering. 

After  drying,  a  5  per  cent,  solution  of  sodium  dioxide  or  sodium 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP.  345 

hydrate  will  accomplish  the  first  requirements.  The  dentine  is  then 
thoroughly  dried  and  saturated  with  cavitine  varnish  containing  hydro- 
naphthol  or  a  solution  of  Canada  balsam  containing  hydronaphthol, 
or  thin  chloro-percha  containing  aristol  or  iodoform,  or  the  formalde- 
hyde preparations  known  as  "Formagen"  and  "  Jodo-Formagen"  may 
be  spread  over  it,  or  oxychloride  of  zinc,  the  fluid  of  which  has  been 
diluted  one-third  with  water,  may  be  used  as  a  covering. 

Williams^  suggests  that  the  decalcified  dentine  be  first  saturated 
with  absolute  alcohol  for  one  minute,  then  dried,  then  wet  with  oil 
of  cloves  for  one  minute,  then  again  dried,  after  which  the  varnish, 
etc.,  is  to  be  used. 

Powdered  sulphate  of  copper  may  be  dusted  over  the  floor  of  the 
cavity  or  used  in  solution  to  saturate  the  dentine,  after  which  the 
dentine  should  be  dried  and  encased  in  varnish. 

The  use  of  these  preparations  obviates  the  necessity  of  sealing 
temporary  antiseptics  in  the  cavity,  as  they  are  in  themselves  more 
or  less  permanently  antiseptic.  Over  them  asbestos  paper  or  thin 
gutta-percha  is  placed  and  then  zinc  phosphate,  made  antiseptic  with 
aristol  or  hydronaphthol,  is  packed,  and  if  any  doubt  exist  the  cavity 
is  temporarily  sealed  with  gutta-percha  or  temporary  stopping.  When 
all  doubt  is  at  rest  the  metal  filling  may  be  placed. 

In  some  cases  of  deep-seated  caries  in  which  gold  filling  is  desirable, 
but  in  which  linings  are  contraindicated,  yet  in  which  immediate 
filling  with  metal  would  involve  such  thorough  excavation  as  to 
endanger  pulp  vitality  either  as  the  result  of  excavation  or  subsequent 
thermal  shocks,  oxychloride  of  zinc  may  be  placed  in  the  peripherally 
prepared  cavities  and  over  considerable  masses  of  decalcified  dentine. 
If  allowed  to  remain  for  several  months  (three  to  six)  the  oxychloride 
stimulates  the  pulp  to  the  formation  of  some  secondary  dentine  and 
complete  excavation  to  a  sound  basis  may  be  made.  There  is  also 
some  evidence  of  hardening  of  the  dentine.  This  method  is  open 
to  the  possible  objection  that  secondary  dentine  is  a  source  of  future 
trouble,  but  the  method  has  its  advantages  in  badly  decayed  anterior 
teeth.^  In  very  deep  cavities  the  fluid  of  the  oxychloride  should  be 
diluted  one-third. 

1  Items  of  Interest,  1898. 

-  In  some  eases  of  this  sort  seen  by  the  writer,  and  observed  for  from  ten  to  sixteen  years, 
the  ill  results  of  oxychloride  of  zinc  claimed  have  not  been  observed.  In  one  case,  after  six- 
teen years  a  lateral  incisor  crown  broke  off,  and  the  pulp  was  found  to  have  receded,  but  was 
otherwise  apparently  healthy.  The  question  is  one  of  the  advisability  of  immediate  de\dtaUza- 
tion,  with  its  advantages  and  disadvantages  in  anterior  teeth,  or  of  a  possible  remote  pulp 
death,  etc. 


346  DENTAL  CARIES. 

In  these  cases  porcelain  inlays  with  their  underlying  cement  should 
have  due  consideration  as  therapeutic  means. 

In  deep  and  very  deep-seated  caries  in  situations  in  which  discolor- 
ation is  not  of  great  moment  the  cavity  may  first  be  lined  with  copper 
amalgam  for  its  antiseptic  value.  This  is  advanced  toward  setting 
by  the  use  of  a  wafer  of  amalgam  from  which  the  mercury  has  been 
expressed.  The  filling  material  is  then  dished  out  so  that  the  ca\dty 
margins  are  freed  of  it.  The  ordinary  amalgam  is  then  added  to 
contour.  Copper  amalgam  alone  ordinarily  becomes  disintegrated 
and  caries  recurs.     Occasionally  it  lasts  well  (especially  Sullivan's). 

Dobrzyniecki^  (Budapest),  in  eight  experimental  cases  upon  micro- 
scopically sound-looking  dentine,  claims  to  have  found  the  bacillus 
gangrense  pulpse  vital  after  months  of  enclosure  under  sealed  dress- 
ings of  camphor,  concentrated  carbolic  acid,  or  eucal}^tus  oil.  All 
other  organisms  w'ere  devitalized.  As  Arkovy's^  experiments  showed 
the  decided  influence  of  carbolic  acid  over  this  organism,  and  as  root- 
canal  antiseptics  are  nearly  always  successful  in  cases  of  moist  gan- 
grene of  the  pulp  (bacillus  gangrense  pulpc^e  Arkovy),  the  difficulty  of 
destroying  this  germ  by  germicides  left  indefinitely  in  the  cavity  must 
be  accepted  with  reservation. 


THERAPEUTICS  OF  EXPOSED  PULP. 

The  exposure  of  the  pulp  may  be  the  direct  result  of  caries;  the 
removal  of  boggy,  disintegrated  dentine  may  produce  it,  or  it  may 
be  the  result  of  the  removal  of  a  last  layer  of  decalcified  dentine  or 
of  the  careless  or  inadvertent  perforation  of  sound  dentine  by  instru- 
ments. Fracture  or  abrasion  are  occasionally  responsible  for  exposure. 
Erosion  rarely  causes  it. 

Diagnosis.  After  excavation  of  the  cavity,  washing  with  tepid  water, 
and  drying,  direct  vision  or  a  reflected  image  in  the  mouth-mirror 
may  reveal  the  area  of  exposure  as  a  round  opening  occupied  by  a 
pinkish  or  red  body.  If  the  exposure  be  large,  pulsation  of  the  red 
body  may  usually  be  observed.  The  exposure  may  be  so  slight  as 
to  be  invisible,  the  depth  of  the  cavity,  however,  indicating  that  expo- 
sure probably  exists.  Bleeding  is  a  certain  guide,  but  bleeding  from 
the  gum  margin  must  be  borne  in  mind.  Truman  ad\ases  in  these 
cases  that  finely  carded  cotton  be  gently  passed  over  the  cavity  walls, 

1  Sbderberg  upon  Arkovy,  Dental  Cosmos,  1899.  -  Ibid. 


THERAPEUTICS  OF  EXPOSED  PULP.  347 

exposure  being  detected  by  the  momentary  pain  produced  when  the 
fibres  pass  over  the  area  of  exposure. 

As  this  test  may  fail  in  cases  of  known  exposure  it  is  not  altogether 
reliable. 

A  finely  pointed  probe  may  be  gently  dragged  over  the  pulpal  wall 
and  catches  in  the  orifice  of  exposure,  however  small.  A  quick  start 
upon  the  part  of  the  patient  is  usually  elicited.  Flagg  warned  against 
requesting  an  affirmative  nod  by  the  patient,  as  this  would  cause 
injury  to  the  pulp.  Delicately  used,  this  test  is  the  most  reliable  in 
all  classes  of  cases  and  is  not  painful. 

It  is  to  be  remembered  that  disease  may  have  caused  a  loss  of  a 
portion  of  a  pulp  horn;  gentle  exploration  will  detect  the  amount 
lost.    Blood,  or  pus  followed  by  blood,  are  evidences  of  exposure. 

Excruciating  pain  following  mastication,  or  pressure  or  suction 
exerted  upon  the  cavity  by  means  of  the  tongue,  are  subjective  symp- 
toms indicating  a  probable  diagnosis  of  exposure. 

Treatment.  An  exposed  pulp  is  either  to  be  capped  or  removed  and 
the  canals  filled. 

The  concensus  of  opinion  is  that  ordinarily  all  pulps  should  be 
removed,  except  those  freshly  exposed  by  removal  of  simply  decalcified 
dentine  and  by  accident.  There  is  no  certainty  that  pulps  exposed 
by  caries  or  practically  so  will  live  under  capping  materials,  but  the 
attempt  may  be  made  at  times  for  special  reasons. 

Freshly  exposed  pulps  may  be  capped  or  removed.  Perhaps  a  good 
rule  would  confine  capping  to  anterior  teeth  of  the  better  grades  in 
patients  in  good  physical  condition,  and  to  pulps  in  teeth  ha\dng 
incomplete  roots.  The  improved  methods  of  pulp  removal  and  canal 
antisepsis  warrant  pulp  destruction  as  a  safer  method  than  capping 
in  most  posterior  teeth.  Even  in  anterior  teeth,  pulp  removal  for 
anchorage  purposes  if  needed  is  quite  warrantable.  The  advantages 
of  capping  are  maintenance  of  tooth  translucency  and  the  avoidance 
of  canal  work. 

The  disadvantages  are:  1.  Possible  death  of  the  pulp  by  hyper- 
eemia  due  to  conduction  of  thermal  changes.  2.  An  overproduction 
of  secondary  dentine  or  the  production  of  pulp  nodules,  the  pulp 
becoming  exhausted  and  death  ensuing.  Increased  difficulty  of  canal 
treatment  may  result.  3.  Disease  of  the  pulp  due  to  infection  beneath 
the  capping  material.  4,  The  time  required  for  assurance  of  success 
or  failure. 

The  object  sought  in  capping  is  the  protection  of  the  pulp  from 


348  DEXTAL  CARIES. 

infection  and  compression,  as  either  is  fatal  to  pulp  vitality.  This 
is  best  accomplished  by  placing  against  the  pulp  and  in  absolute 
contact  with  it  an  antiseptic  paste  beneath  a  metal  cap,  or  an  anti- 
septic cement  having,  when  set,  sufficient  rigidity  to  permit  other 
work  to  be  done. 

Prognosis  is  favorable  for  the  cases  selected  as  suggested. 

Pulp  Capping.  The  cap  should  be  made  of  platinum  or  gold  for 
anterior  teeth.  Tin,  lead,  or  silver  may  be  used  posteriorly.  After 
punching  or  trimming  to  shape  it  should  be  made  concavo-convex 
by  pressing  it  into  soft  wood  by  means  of  the  rounded  end  of  an 
instrument  handle.  A  film  of  wax  is  placed  on  the  convex  side; 
a  warmed,  small  burnisher  is  attached,  and  the  cap  is  adjusted  in 
proper  position  by  trying  in  the  cavity.  It  is  then  to  be  filled  with 
the  capping  material  (a  little  of  the  latter  placed  in  any  depression 
at  the  point  of  exposure  in  order  to  exclude  air) ;  then  one  side  of  the 
cap  is  laid  upon  the  dentine  and  the  other  gradually  brought  down, 
and  the  edges  of  the  cap  firmly  adapted  to  the  dentine.  This  causes 
the  paste  to  exude  from  beneath  the  cap.  Any  excess  is  gently  removed 
with  an  excavator.  A  little  "cavitine"  varnish  or  chloro-percha  is  to 
be  placed  over  the  pulpal  wall  and  cap  and  dried.  A  little  soft 
cement  is  now  placed  over  the  varnish  as  a  protection,  and  when  set 
the  filling  is  completed  with  gutta-percha  or  zinc  phosphate  cement, 
which  is  to  be  allowed  to  remain  a  year  as  a  test  of  success. 

These  may  be  renewed  as  worn  out  if  desirable,  or  a  portion  of 
the  covering  filling  may  be  cut  away  and  metal  introduced.  In  case 
a  plastic  filling  is  desirable  in  any  event,  the  operation  is  to  be  com- 
pleted at  the  time  of  capping  or  at  a  subsequent  sitting. 

The  materials  used  with  success  as  pulp  cappers  are :  1 .  A  mixture 
of  oil  of  cloves  and  zinc  oxide  (equal  parts  of  carbolic  acid  and  oil 
of  cloves  may  be  used  as  the  menstruum).  Hubbuck's  zinc  oxide  or 
cement  powder  may  be  used.  This  is  mixed  to  a  consistency  which 
will  flow  yet  set  in  time 

2.  Oxysulphate  of  zinc,  the  fluid  of  which  is  a  saturated  solution  of 
zinc  sulphate  in  water.  The  powder  is  uncalcined  zinc  oxide.  This 
will  make  a  thin,  creamy  paste  which  flows  readily  and  sets  quickly. 
A  trifle  of  aristol,  iodoform,  or  hydronaphthol  may  be  added. 

3.  Plaster  of  Paris  mixed  with  a  1  per  cent,  solution  of  formaldehyde 
in  water  will  make  an  antiseptic,  quick-setting  paste. 

4.  "  Formagen."  This  substance  is  said  to  have  a  mixture  of 
eugenol  and  carbolic  acid  for  the  fluid,  while  the  powder  is  of  zinc 


THERAPEUTICS  OF  PERFORATION  BY  CARIES.  349 

oxide,  containing  paraform,  the  solid  form  of  formaldehyde.  A  cement 
is  formed  which  sets  quickly  and  must  therefore  be  made  very  thin 
when  placed  in  the  cap.  This  material  seems  to  have  been  somewhat 
successful  as  a  capper  even  in  exposures  by  caries,  owing  to  its  intense 
germicidal  power.  It  is  claimed  that  the  formaldehyde  penetrates  the 
tissue  of  the  pulp  for  a  distance,  yet  permits  its  return  to  normality. 

Results  of  Capping.  If  pain  be  initiated  when  the  cap  is  placed 
and  recur  later,  compression  has  occurred  and  the  capping  must  be 
removed,  the  pulp  quieted,  and  the  capping  renewed  or  the  pulp 
removed.  Though  no  sensation  be  produced  at  the  time  of  operation 
a  reaction  to  thermal  changes  may  occur.  If  this  gradually  subside 
as  counterirritants  are  used,  a  diagnosis  of  arterial  hypersemia  (aseptic) 
is  confirmed.  If  the  reaction  increase  and  heat  become  more  irritating 
than  cold,  and  if  at  the  same  time  paroxysms  of  pain  or  reflex  pain 
occur,  the  diagnosis  is  that  of  venous  hyperaemia  or  infective  inflam- 
mation, according  to  the  charac!;er  of  the  symptoms,  and  the  pulp 
must  be  removed. 

A  pulp  may  remain  quiescent  for  weeks  or  months  and  then  un- 
favorable symptoms  set  in,  or  it  may  die  without  any  apparent  pain. 
It  is  probable  that  in  the  latter  case  some  reflex  pains  have  been  felt, 
but  not  related  with  the  tooth,  in  the  mind  of  the  patient. 

In  the  successful  cases,  either  the  orifice  of  exposure  is  covered  over 
by  a  deposit  of  secondary  dentine,  or  the  pulp  remains  perfectly 
quiescent  beneath  the  capping  material,  without  formation  of  deposit. 

Even  when  a  deposit  occurs  the  pulp  may  die  from  the  atrophy 
and  degeneration  attendant  upon  the  formation  of  much  secondary 
dentine,  and  when  no  deposit  occurs  infection  following  leakages 
about  filling  and  capping  materials  may  take  place  after  years  of 
apparent  success. 

While  capping  may  be,  and  has  been,  successful  in  all  grades  of 
exposure,  there  is  no  certainty  of  success  in  the  exposures  by  caries. 
The  tentative  treatment  necessary  offsets  the  labor  of  canal  treatment. 

THERAPEUTICS  OF  PERFORATION  BY  CARIES. 

The  progress  of  secondary  caries  about  the  pulp  chamber  hollows  out 
the  root  until  at  least  at  one  point  the  chamber  wall  is  but  a  decalcified 
layer  of  cementum  covered  by  decomposing  dentine.  At  some  point 
the  pericemental  tissue  will  be  uncovered  by  excavation  or  by  the  carious 
process  (Fig.  320).     The  crown  will  probably  be  hopelessly  decayed. 


350  DENTAL  CARIES. 

Taking  as  an  example  a  lower  molar  perforated  at  the  bifurcation 
with  the  pericemental  tissue  hypertrophied  into  the  opening  (fungous 
gum),  its  treatment  may  be  described  as  follows:  The  gum  is  first 
to  be  pressed  out  with  cotton  medicated  with  an  antiseptic  varnish. 
Fletcher's  carbolized  resin,  or  aristol  in  chloroform,  or  sandarac 
varnish  plus  orthoform  will  serve,  or  temporary  stopping  may  be  used. 
If  immediate  work  be  desired  the  fungous  gum  may  be  saturated 
with  trichloracetic  acid  and  cut  away  without  bloodletting  by  means 
of  a  large,  sharp,  spoon  excavator.  Large,  rose-head  burs  are  used  to 
free  the  cavity  of  all  decay.  The  canals  are  opened  and  treated.  If 
further  treatment  be  desired,  or  be  impossible  until  the  perforation 
is  disposed  of,  metal  or  wooden  pegs  are  placed  in  the  canals  and  a 
reasonably  thin  layer  of  copper  amalgam  is  built  about  the  pins  and 
over  the  perforation.  A  slight  movement  of  the  pegs  will  permit  their 
withdrawal,   leaving  openings  in  the  amalgam  through  which  the 

Fig.  334. 


0^**^- 


Diagram  of  treatment  of  perforation  Crowning  of  divided  roots.      (Evans.) 

by  decay. 

treatment  may  be  conducted.  The  amalgam  is  then  allowed  to  harden 
(Fig.  333). 

After  canal  filling  the  canals  may  be  further  reamed  for  screws  or 
pins,  which  are  inserted  and  the  operation  completed  wdth  amalgam 
or  zinc  phosphate  if  the  condition  of  the  crown  admit  of  it;  or,  if  crown- 
ing be  required,  this  is  arranged  for  in  the  building  up  with  amalgam. 

A  long  perforation  at  a  bifurcation  may  practically  divide  molar 
roots.  This  is  to  be  made  a  complete  division  after  treatment  of  the 
canals.  Each  section  may  be  fitted  with  a  pin  and  amalgam  stump 
to  which  a  gold  barrel  is  fitted.  The  barrels  are  each  given  an 
occlusal  face  and  soldered  together  (Fig.  334). 

A  smooth  plaque  of  low-heat,  white  gutta-percha  (not  temporary 
stopping)  makes  an  excellent  covering  for  a  perforation.  It  is  made 
larger  than  the  opening  to  be  covered,  pressed  to  place,  and  the  edges 


CARIES  OF  THE  TEMPORARY  TEETH.  35I 

sealed  with  a  hot  burnisher.     The  covering  filhng  will  retain  it  in 
position. 

In  all  cases  judgment  must  be  exercised  and  the  attempt  to  conserve 
unsuitable  cases  avoided. 


THERAPEUTICS  OF  LOSS  OF  CROWN  BY  CARIES. 

If  the  portion  of  crown  left  after  excavation  be  self-sustaining,  but 
incapable  of  retaining  a  filling,  pins  or  screws  may  be  placed  in  the 
root  canal  or  the  pulp  cavity  may  be  enlarged  and  made  retentive. 
A  filling  is  then  built  about  or  into  the  anchorage  so  made.  At  times 
the  remainder  of  a  tooth  crown  will  support  a  hollow  metal  crown. 

When  the  carious  crown  has  broken  away  or  filling  has  become 
practically  impossible  or  undesirable,  the  original  beauty  or  useful 
form  of  the  tooth  may  be  approximately  restored  by  means  of  one  of 
the  many  forms  of  dowelled  porcelain  crowns,  specially  constructed 
gold  and  porcelain  crowns,  or  all-gold,  hollow-metal  crowns. 

If  an  anterior  root  be  so  hollowed  out  by  caries  as  to  be  incapable 
of  supporting  a  dowelled  crown  it  may  be  extracted  and  the  operation 
of  transplantation  performed,  or,  later,  an  implantation  may  be  made. 

In  the  former  operation  the  existing  alveolus  is  enlarged  if  necessary 
to  accommodate  a  tooth;  in  the  latter  operation  a  new  alveolus  is  cre- 
ated by  means  of  appropriate  trephines  and  reamers.  The  tooth  is  to 
be  prepared  as  for  replantation  (which  see).^ 

If  teeth  have  been  lost  by  extraction,  the  spaces  created  may  be 
filled  by  means  of  bridge-work  or  plates  of  various  sorts. 

By  common  consent  crown  and  bridge  work  is  considered  a  special 
department  of  dentistry. 

CARIES  OF  THE  TEMPORARY  TEETH. 

Caries  of  the  temporary  teeth  differs  but  little  from  that  of  the 
permanent  teeth.  The  pulp  cavities  are,  however,  relatively  larger 
and  the  intensity  of  the  carious  process  often  causes  rapid  exposure 
of  the  pulp.  Owing  to  the  flat  character  of  the  approximations  of 
the  teeth  there  is  often  more  proximal  than  occlusal  caries  and  the 
cavities  often  have  weak  peripheries. 

Children  have  a  fear  of  dental  oflEices,  excited  by  unpleasant  experi- 
ences or  the  talk  of  their  elders,  and  they  do  not  mention  slight  pain 

1  For  methods  of  implantation  see  American  Text-book  of  Operative  Dentistry. 


352  DENTAL  CARIES. 

such  as  that  excited  by  hypersensitive  dentine.  There  is,  however, 
abundant  evidence  that  the  dentine  of  the  temporary  teeth  may  be 
hypersensitive. 

In  cavities  of  simple  nature  the  filhngs  indicated  for  adults  serve 
if  the  operations  are  well  borne. 

The  shapes  of  the  teeth,  the  restlessness  and  fear  of  the  little  patients, 
and  the  free  flow  of  saliva  indicate,  for  the  most  part,  the  use  of  plastic 
fillings,  though  the  rubber-dam  may  often  be  readily  used.  In  deep 
cavities  not  exposing  the  pulps  the  methods  employed  for  adults,  of 
varnishing  or  insulating  with  gutta-percha  and  the  subsequent  use 
of  zinc  phosphate  as  a  lining  under  metal  fillings,  are  indicated. 
Certain  occlusal  cavities  having  small  orifices  and  large  interiors  are 
well,  and  often  permanently,  filled  with  pink  gutta-percha. 

If  cavities  are  observed  before  pain  has  been  complained  of,  and 
prompt  and  quickly  subsiding  response  to  applications  of  cold  water 
is  obtained,  indicating  a  normal  pulp,  the  cavity  should  be  excavated, 
with  more  regard  to  removing  the  marginal  caries  than  to  thorough 
excavation,  dried,  and  an  application  of  a  20  per  cent,  solution  of 
silver  nitrate  made  for  a  few  minutes,  the  cavity  being  subsequently 
filled. 

In  cases  of  adjoining  approximal  cavities  there  is  a  disposition  fcr 
the  affected  teeth  to  press  together  and  lessen  the  size  of  the  dental 
arch.     Bonwill  advised  as  a  practice,  followed  by  uniformly  good 
results  in  such  cases,  to  cleanse  the  cavities  (Fig.  335)  and  insert 
masses  of  pink  gutta-percha  base-plate.     The  con- 
stant biting  upon  the  gutta-percha  causes  a  separa- 
tion of    the  teeth,  which  increases  the  size  of    the 
arch  and  affords    additional  space  for   permanent 
successors.      He    advised    that    before    the    gutta- 
percha masses    are    inserted  small  pieces  of    blot- 
ting-paper   saturated   with    carbolic    acid    be    laid 

Mode  of  preparing  ap-  .  i  •       i  n  i    _,i  ,,  i        i 

proximal  cavities.  agauist  the  dentuial  walls  and  the  gutta-percna  be 
packed  over  them.  The  more  efficient  and  per- 
sistent antiseptic  silver  nitrate  may  be  applied  instead  of  the  car- 
bohc  acid.  Kirk  advises  that  asbestos-felt  be  heated  to  destroy  any 
organic  matter  present  in  it  which  might  combine  with  the  silver^ 
and  then  be  soaked  in  a  saturated  solution  of  silver  nitrate,  dried, 
and  kept  in  dark  bottles  away  from  the  light.  Small  pieces  of  the 
prepared  felt  may  be  used  as  described. 

The   silver   nitrate   method   is   particularly  applicable   to   shallow 


CARIES  OF  THE  TEMPORARY  TEETH.  353 

cavities  in  which  excavation  for  filhng  is  impracticable.  The  dentine 
surface  is  cleansed  and  dried,  and  the  fused  silver  nitrate  is  rubbed 
upon  the  surface.  This  may  be  done  after  the  method  of  Craven: 
a  platinum  wire  is  dipped  into  the  powdered  salt  and  held  over  a 
flame  until  the  powder  fuses  into  a  button.  By  this  means  applications 
can  be  directly  and  accurately  made. 

Combination  fillings  of  zinc  phosphate  and  amalgam  are  of  advan- 
tage in  case  of  frail  walls. 

For  the  anterior  teeth  zinc  phosphate  and  gutta-percha  fillings  are 
useful,  and  for  the  posterior  ones  Ames'  oxyphosphate  of  copper 
serves  a  good  purpose. 

Caries  is  very  liable  to  occur  upon  the  proximal  surfaces  of  the 
second  temporary  and  first  permanent  molar.  If  the  former  be  found 
largely  decayed  distally,  the    latter  will  ^^^  ^^^ 

usually  be  found  decayed  on    the  mesal 
surface. 

Well-contoured    fillings    must    be    in- 
serted in  such  a  case.     As  a  preventive  //  /f'  \\  \\  Vv--jV.-r3  N 
measure    during    eruption    of    the    first  ••kif"    '~%:.]j    '"^-— .-'  ''•—"'' 
molar,    the     second     temporary    molar  >  \      J) 
may  be  disked  to  the    form  shown  in  ^--::::--'' 

''  Impingement   of   permanent    molar 

Fig.  336.  upon  the  distal  wall  of  the  temporary 

K'     •        ,  •  1  1  1  second  molar. 

incipient    or    simple    decay   have 

occurred  on  the  two  teeth,  or  even  the  second  molar  alone,  this  form 

will  be  impossible. 

It  is  then  better  to  wedge  the  teeth  apart  and  to  make  the  disk 
separation  (on  the  temporary  tooth  only)  from  the  lingual  or  buccal 
side,  or  both,  and  to  contour  the  filling  even  in  exaggeration,  so  that 
a  minimum  of  contact  shall  exist.  Any  surface  of  dentine  exposed 
by  the  disking  should  be  included  in  the  cavity,  or,  if  this  be  not 
possible,  then  it  should  be  rubbed  with  silver  nitrate  (Fig.  337). 

Such  surfaces  should  be  carefully  observed  at  regular  intervals; 
indeed,  if  prophylactic  treatment  can  be  regularly  instituted  early  and 
before  caries  of  the  first  permanent  molar,  much  good  will  be  done. 

The  pulp  diseases  resulting  from  caries  of  the  temporary  teeth  will 
be  considered  with  those  of  the  permanent  teeth.  If  the  temporary 
teeth  be  so  badly  decayed  as  to  be  hopeless,  as  far  as  filling  is  con- 
cerned, they  should  be  extracted.  Occasionally  the  encircling  of  the 
teeth  with   pure  gold    bands    cemented    to   place   or   filled   in   with 

amalgam  is  good  practice. 

23 


354  DENTAL  CARIES. 

The  child  should  always  be  treated  with  kindness  and  truthfulness 
to  establish  faith,  yet  with  sufficient  firmness  to  command  control. 

Fig.  337. 


Right  upper  temporary  molar  disked  lingually  and  filled. 

Under  no  circumstances  should  the  child  be  given  an  excessive 
dread  of  dental  operations,  or  be  broken  by  nervous  shock,  as  this 
attitude  defeats  the  object  sought. 

RECURRENCE  OF  CARIES. 

Passing  over  as  disproved  by  Miller  the  theory  of  Palmer  that  caries 
recurs  about  fillings  as  the  result  of  electric  action,  it  may  be  stated 
as  proven  by  scientific  and  clinical  experience  that  it  recurs  because 
after  teeth  have  been  filled  conditions  exist  which  favor  the  collection 
of  microbic  plaques  even  more  strongly  than  the  original  conditions, 
and  that  when  recurrence  has  been  prevented  the  work  has  been  done 
in  such  a  manner  as  to  prevent  such  collections. 

The  specific  defects  which  favor  the  formation  of  bacterial  plaques 
may  be  epitomized  as  follows: 

1.  Lack  of  proximal  contact  (food  wedging  between  teeth). 

2.  Roughness  of  the  filling  at  an  otherwise  good  proximal  contact 
point  which  menaces  the  proximating  tooth  or  the  margin  of  the 
cavity. 

3.  Unremoved  excess  of  filling  material  at  margins,  producing  a 
ledge  which  collects  food,  etc.  The  edge  of  a  crown  may  act  in  a 
similar  manner. 


PROPHYLAXIS  OF  CARIES.  355 

4.  Exposure  of  the  cavity  margin  due  to  lack  of  covering  by  the 
filling  material;  whether  not  properly  placed,  flaked  away,  or  due  to 
fracture  of  margin  during  the  filling  process  or  subsequently  thereto. 

5.  Exposure  of  the  cavity  margin  due  to  shrinkage  or  shifting  of 
the  filling  material. 

6.  Roughness  of  tooth  surface,  produced  by  polishing  fillings  with 
rough  proximal  trimmers,  coarse  grit  strips,  disks,  or  wheels.  Exposure 
of  dentine  by  overpolishing  may  be  classed  with  the  above. 

7.  Lack  of  extension  of  cavity  margins  to  a  point  which  brings 
them  within  the  influence  of  ordinary  prophylactic  measures  or  forces. 

8.  Lack  of  hygiene  of  surfaces  which  tend  to  decay. 

9.  Solubility  of  the  filling  material,  permitting  the  cavity  wall  to 
become  exposed. 

Treatment.  The  treatment  of  recurrent  caries  does  not  differ 
materially  from  that  of  primary  caries. 

Repairs  to  obliterate  crevices,  breaks,  or  new  decays  may  at  times 
be  made,  but  so  often  is  it  the  case  that  apparently  slight  recurrences 
are  found  after  removal  of  the  filling  to  involve  the  entire  cavity  wall, 
that  the  only  sound  recommendation  applicable  to  all  cases  is  that 
the  filling  be  removed  and  the  cavity  reprepared  and  refilled.  The 
exception  exists  when,  after  the  new  cavity  of  decay  is  all  excavated, 
the  adaptation  of  the  filling  is  seen  to  be  perfect.  Decay  at  two  or 
more  points  of  recurrence,  or  general  inferiority  of  the  filling  should 
condemn  the  entire  piece  of  work. 

PROPHYLAXIS  OF  CARIES. 

If  the  factors  of  caries  be  removed  from  the  mouth,  caries  cannot 
occur.  That  a  clean  tooth  will  not  decay  is  a  dictum  many  years 
established.  That  the  caries  fungi  may  be  present  in  the  mouth  and 
be  harmless,  unless  conditions  favor  the  formation  of  gelatinous 
plaques  upon  the  teeth,  has  been  shown  by  Black  and  Williams. 

These  facts  demonstrate  that  the  sole  requirement  in  the  prevention 
of  caries  is  the  prevention  of  the  formation  of  gelatinous  plaques 
upon  spots  favoring  their  retention. 

It  has  been  shown  by  Williams  that  caries  is  a  reasonably  slow 
process;  therefore,  the  removal  of  plaques  at  frequent  intervals  is 
sufficient  for  the  prevention  of  caries. 

In  the  absence  of  exact  knowledge  of  the  relation  of  general  systemic 
conditions  to  the  production  of  these  plaques,  it  may  be  said  that  the 


356  DENTAL  CARIES. 

general  health  should,  if  possible,  be  maintained  bv  the  correction 
of  any  morbid  body  state,  as,  without  doubt,  perfect  good  health  is 
a  corrective  of  morbid  oral  secretions. 

Apart  from  this,  oral  cleanliness  is  of  great  importance,  not  only 
for  the  health  of  the  teeth,  but  of  the  gums,  and  indirectly  of  the 
stomach  and  intestines,  which  can  but  be  affected  by  unhealthy  oral 
conditions.  Thus,  while  the  general  health  may  influence  the  mouth, 
the  mouth  may  influence  the  general  health. 

It  has  been  noted  that  caries  is  markedly  lessened  in  well-kept 
dentures. 

The  first  step  in  the  prevention  of  caries  is  the  removal  of  all  possible 
causes  of  bacterial  plaque  formation.  Cavities  should  be  obliterated 
by  means  of  exactly  adapted,  perfectly  contoured,  highly  polished, 
insoluble  (in  so  far  as  utilizable)  fillings,  the  margins  of  which  are 
extended  into  areas  subjected  to  friction  by  ordinary  means.  Depart- 
ures from  this  principle  are  to  be  made  for  well-judged  reasons  only. 
By  these  means  centres  of  infection  are  removed  and  the  problem 
is  reduced  to  the  care  of  the  superficies  of  the  teeth.  Calculus  should 
be  thoroughly  removed,  the  teeth  highly  polished  and  kept  polished. 
This  operation  mechanically  removes  the  plaques. 

To  prevent  their  return,  daily  cleansing  of  the  teeth  by  the  patient 
has  always  been  practised,  and  a  thorough  cleansing  once  a  month 
or  oftener  by  the  operator  has  been  shown  by  D.  D.  Smith  to  be 
highly  efficacious. 

DAILY  CLEANSING  OF  THE  TEETH. 

A  well-made,  stiff  brush,  ha\ing  a  lengthened  tuft  of  bristles 
at  its  tip  and  its  brushing  surface  serrated,  is  to  be  moistened 
and  well  charged  with  a  good  antiseptic  tooth-powder  or  paste.  It 
is  to  be  grasped  in  the  palm  of  the  hand  with  the  ball  of  the  thumb 
placed  upon  the  back  of  the  handle,  or  exactly  the  reverse,  according 
to  the  movement  desired.  The  bristles  are  to  be  passed  over  the 
buccal  and  lingual  surfaces  of  the  teeth,  from  the  gum  toward  the 
occlusal  surfaces,  by  means  of  a  dexterous,  wiping  motion  imparted  by 
a  turn  of  the  wrist.  This  cleanses  the  interproximal  spaces  so  far  as 
accessible  to  it.  By  a  light  to-and-fro  motion  the  lingual  and  buccal 
crevices  are  freed  of  soft  deposits  which  occur  after  each  meal.  Unless 
the  gums  be  actually  torn,  this  light  friction  is  not  injurious.  Especial 
attention  is  to  be  paid  to  the  buccal  surfaces  of  third  molars,  which 
are  often  ignored  even  by  conscientious  patients. 


DAILY  CLEANSING  OF  THE  TEETH.  357 

The  lingual  surfaces  of  incisors  are  cleansed  by  means  of  the  stiff 
tip  of  the  brush.  In  cases  of  advanced  recession  of  the  gum  about 
incisors,  a  brush  with  all  the  bristles  except  those  of  the  tip  cut  away 
is  advantageous.  This  is  also  useful  for  the  lingual  surfaces  of  bridge 
work.     Occlusal  surfaces  are  to  be  freely  brushed. 

A  light  brushing  after  each  meal  imparts  to  the  mouth  a  pleasing 
sense  of  cleanliness  which  has  a  good  moral  effect  upon  the  patient 
and  removes  from  about  the  teeth  much  fermentable  material. 

The  teeth  should  be  thoroughly  brushed  upon  retiring  to  remove 
any  debris  about  the  teeth,  and  the  antiseptic  and  antacid  treatment 
to  be  mentioned  employed.  This  places  the  mouth  in  a  fairly  aseptic 
state  for  the  night,  during  which  the  oral  fluids  are  at  rest  and  less 
interfere  with  fermentation  or  neutralize  its  products. 

Before  breakfast  the  mouth  should  again  be  treated  to  remove  the 
bacteria  developed  during  the  night. 

Once  a  week  the  patient  should  dip  floss  silk  in  the  tooth-powder 
(or  rub  the  powder  over  the  interproximal  spaces),  carry  it  between 
the  teeth  and  rub  down  the  proximal  surfaces,  with  the  object  of 
removing  any  bacterial  collection  upon  these  surfaces. 

The  floss  silk  should  not  be  forced  into  the  gum,  as  this  will  injure 
the  gum  margins  and  force  infective  material  into  it. 

After  cleansing  the  teeth  an  antiseptic  should  be  held  in  the  mouth 
for  the  space  of  two  minutes,  for  the  purpose  of  devitalizing  bacteria 
present.  For  this  purpose  phenol-sodique  in  25  per  cent,  solution  in 
water  (1  to  3)  is  as  valuable  as  any  agent,  though  many  harmless 
preparations  are  sold  for  this  purpose.  Perhaps  glycothymolin,  being 
alkaline  and  antiseptic  as  well  as  agreeable,  is  to  be  preferred. 

In  a  mouth  especially  prone  to  caries  of  the  teeth  it  is  well  to  use, 
once  or  twice  a  week,  a  disguised  mercuric  chloride  wash  1 :  2000 
for  the  space  of  two  minutes.  The  object  is  to  thoroughly  devitalize 
oral  organisms  and  promote  the  action  of  the  milder  and  more  agree- 
able antiseptics. 

Finally,  after  the  above  treatment,  Phillips'  milk  of  magnesia 
(magnesium  hydrate  in  suspension)  should  be  taken  in  concentrated 
form  into  the  mouth,  rinsed  about  and  drawn  by  suction  between  the 
teeth.  The  excess  is  to  be  expectorated  and  the  residue  left  in  the 
mouth.  It  is  alkaline,  slightly  astringent,  and  is  credited  with  some 
antiseptic  property.  These  processes  do  not  consume  much  time  if  the 
patient  be  systematic. 

The  periodical  cleansing  suggested  by  D.  D.  Smith  involves  the 


358  DENTAL  CARIES. 

monthly  rubbing  down  of  all  surfaces  accessible  to  a  wedge-shaped 
wooden  polishing  point  directed  by  a  hand  carrier.  Powdered  pumice 
is  the  abrasive  suggested.  The  point  is  to  be  gently  insinuated  beneath 
the  free  gum  margin  for  the  purpose  of  effecting  a  cleanliness  there, 
which  shall  prevent  collections  liable  to  produce  pyorrhoea  alveolaris. 

This  method  may  be  supplemented  by  a  careful  rubbing  down  of 
contact  points  by  means  of  floss  silk  charged  with  powdered  pumice 
as  an  additional  precaution  against  proximal  caries. 

The  slight  cleansing  apparently  required  after  a  few  visits  is  a 
strong  argument  in  favor  of  these  prophylactic  cleansings. 

Periodical  examinations  should  be  made  at  short  intervals,  pref- 
erably at  the  time  of  cleansing,  for  cavities  of  decay,  roughness  of 
filling  margins,  or  accidents  to  the  same.  By  these  means  the  soil 
may  be  rendered  unsuitable  to  the  growth  of  caries  fungi. 

Some  dentists  pursue  the  policy  of  filling  only  the  larger  cavities 
existing  in  a  mouth,  the  others  being  neglected  until  a  subsequent 
period.  Such  a  method  is  to  be  condemned  as  being  a  neglect  of  a 
plain  duty  and  as  tending  to  the  propagation  of  caries  in  the  mouth. 
The  presence  of  cavities,  calculus  and  pyorrhoea  alveolaris  in  the 
mouth  all  tend  to  cause  infection  of  the  digestive  tract,  with  produc- 
tion of  inflammatory  (catarrhal)  disturbance,  and  to  cause  infection 
of  parts  in  close  association  with  the  teeth  as  well. 

Undoubted  cases  of  septic  intoxication  and  infection  from  decayed 
teeth  and  other  oral  conditions  have  been  reported,  the  connection 
having  been  shown  by  their  cure  after  removal  of  the  local  cause 
alone;  in  other  cases  the  parts  (as  the  stomach)  having  the  second- 
ary infection  well  implanted,  have  required  special  antiseptic  treat- 
ment in  addition  to  the  removal  of  the  primary  exciting  cause.^  (See 
Systemic  Effects  of  Pyorrhoea  Alveolaris.) 

The  evils  attendant  upon  sepsis  are  to  be  pointed  out  to  patients, 
who  have  often  a  seeming  indifference  to  conditions  within  the  mouth 
which  would  alarm  them  if  existing  in  any  other  part  of  the  body. 

PROPHYLAXIS  IN  SYSTEMIC  DISEASE. 

During  a  prolonged  illness,  seasickness,  pregnancy,  etc.,  the  prophy- 
lactic care  of  the  teeth  should  be  rigidly  enforced  as  a  means  of  pre- 
venting decay  of  the  teeth  and  sepsis  of  the  mouth. 

1  Hunter,  International  Dental  Journal,  1899.  Abstract  from  Transactions  of  Odontological 
Society  of  Great  Britain. 


PROPHYLAXIS  IN  SYSTEMIC  DISEASE.  359 

It  has  been  shown  that  during  pregnancy  osteomalacia-  may  occur 
and  that  it  represents  a  deminerahzation  of  the  bones  of  the 
mother.  Whether  or  not  this  may  influence  caries  of  enamel  is  not 
certain,  but  there  is  no  reason  why  the  resistance  of  the  fibrillse 
of  the  dentine  should  not  be  lessened,  or  even  that  the  dentine  may 
not  be  to  an  extent  demineralized,  as  positively  claimed  by  some 
accurate  observers  (Black  to  the  contrary) .  An  excessive  osteomalacia 
may  be  held  to  represent  a  deficiency  of  osteogenetic  nutritive  material 
for  the  child.  This  would  lead  to  an  inferior  development  of  the 
child's  teeth. 

Any  abnormal  condition  of  the  mother  should  be  corrected,  if 
possible,  in  order  that  her  general  nutrition  and  that  of  the  child 
may  not  suffer. 

Probably  upon  the  congenital  constitution  of  the  child  depends 
much  of  its  future  susceptibility  or  immunity  to  caries. 


SECTION  lY. 

DISEASES  OF  THE  DENTAL  PULP. 


CHAPTER   XVI. 

CONSTEUCTIVE  DISEASES. 

Diseases  of  the  dental  pulp  are  both  acute  and  chronic.  Accord- 
ing to  the  anatomical  features,  they  may  also  be  di^dded  into  con- 
structive and  destructive.  The  acute  diseases  are  usually  destruc- 
tive; in  the  chronic,  structural  and  constructive  changes  are  commonly 
noted.  Constructive  diseases  of  the  dental  pulp  are  those  attended  by 
the  formation  of  deposits  of  new  masses  of  calcific  substance.  De- 
structive diseases  are  those  which  cause  retrogressive  and  necrotic 
changes  in  the  tissues  of  the  pulp.  The  essential  difference  between 
the  two  classes  of  diseases  is  in  the  mode  and  character  of  the  degen- 
eration— the  one  is  acute,  the  other  chronic. 

Pathologically  there  is  no  abrupt  line  of  separation  between  those 
disorders  usually  termed  diseases  of  the  dental  pulp  and  those  which 
are  described  under  the  head  of  diseases  of  the  live  dentine.  As  soon 
as  the  dentine  of  the  crown  of  a  tooth  is  deprived  of  a  portion  of  its 
normal  protective  covering,  the  enamel,  either  through  chemical 
solution  incident  to  the  first  phase  of  dental  caries  or  from  mechanical 
abrasion,  the  vital  portions  of  the  dentine  are  subjected  to  new  and 
abnormal  conditions.  These  vital  portions  being  in  reahty  prolon- 
gations of  the  peripheral  cells  of  the  pulp,  it  is  e\'ident  that  the  morbid 
conditions  engendered  by  their  exposure  are  expressions  of  pulp 
disturbance,  and  we  should  expect  to  find  reactionary  effects  upon 
the  part  of  the  pulp.  Depending  upon  the  severity  of  the  irritation 
and  the  length  or  number  of  times  sources  of  irritation  have  been 
in  operation,  e\adences  of  functional  and  structural  disorders  in  the 
body  of  the  dental  pulp  are  observ^ed. 

Post-mortem  knowledge  of  structural  diseases  of  the  dental  pulp  is 
comparatively  complete,  but  a  parallel  knowledge  of  the  exact  nature 


362  CONSTRUCTIVE  DISEASES. 

of  the  causes  producing  definite  and  recognizable  conditions,  together 
with  the  symptoms  which  precede  and  accompany  the  several  morbid 
states,  is  incomplete.  In  the  absence  of  precise  information  as  to  the 
association  between  disease  causes,  their  symptoms  and  effects,  physio- 
logical and  pathological,  the  practitioner  bases  his  diagnosis  of  the 
anatomical  condition  of  the  pulp  on  symptoms  which  he  is  enabled 
to  elicit  by  certain  tests,  and  by  the  history  furnished  by  the  patient. 
The  tests  applied  and  histories  obtained  direct  attention  to  the  vascular 
system  of  the  pulp  as  the  primary  cause  of  many,  or  most,  of  the 
conditions  of  the  organ  which  are  attended  by  paroxysmal  and  reflex 
pains.  The  reactions  to  tests  occur  both  with  and  without  exposure 
of  the  pulp  to  external  sources  of  bacterial  infection,  although  they 
are  found  in  the  vast  majority  of  cases  where  bacterial  invasion  is 
a  probability. 

SYMPTOMATOLOGY  OF  THE  PULP. 

Writers  upon  dental  pathology,  during  at  least  the  past  twenty-five 
years,  have  called  attention  to  the  fact  that  pain  produced  through 
the  irritation  of  the  dental  pulp  is  rarely  referred  to  its  point  of 
origin;  that  is,  diseases  of  the  pulp  are,  as  a  rule,  characterized  by 
reflected  pains.  G.  V.  Black  has  clearly  set  forth  the  causes  and 
reason  of  this  phenomenon.  "The  pulp  of  a  tooth  is  not  its  tactile 
organ;  that  is,  it  does  not  possess  the  sense  of  location.  The  only 
stimulus  to  which  it  responds  in  its  normal  state,  when  encased  in  an 
unbroken  chamber  of  dentine,  which  is  perfectly  sheathed  with  enamel, 
is  applications  of  heat  or  cold.  Far  removed  in  its  normal  state  from 
situations  in  which  a  tactile  sense  could  perform  any  physiological 
function,  such  a  sense  would  be  useless.  Organs  in  which  the  tactile 
sense  is  absent,  and  in  which  it  would  be  perhaps  superfluous,  when 
the  seat  of  disease  have  the  pain  incidental  to  the  disease  reflected  to 
other  parts;  for  example,  in  hip-joint  disease,  pain  at  the  inner  side 
of  the  knee  is  a  diagnostic  sign;  in  inflammations  of  the  iris  the  pain 
is  referred  to  the  brow;  pain  at  the  orifice  of  the  urethra  is  indicative 
of  disease  of  the  bladder,  and  so  on.  So  with  irritation  of  the  dental 
pulp,  the  pain  is  indefinitely  or  vaguely  located.  In  those  cases  where 
pain  is  referred  to  the  tooth  irritated,  there  are  associated  conditions 
which  produce  a  response  of  the  true  tactile  organ  of  the  tooth,  the 
pericementum." 

The  pathological  conditions  of  the  pulp  are  judged  by  the  phenom- 
ena induced  by  applications  of  air  or  water  of  varying  temperatures, 


SYMPTOMATOLOGY  OF  THE  PULP.  363 

and  by  the  presence  of  certain  appearances  of  the  tooth,  which,  taken 
with  the  symptoms  and  tests,  lead  to  a  fair  inference  of  the  disease 
present. 

It  was  pointed  out  by  Black^  that  if  a  healthy  tooth  be  isolated  by 
a  double  layer  of  rubber-dam,  and  a  jet  of  water  at  a  temperature  of 
40°  F.  be  directed  against  the  tooth,  a  paroxysm  of  pain  is  produced. 
A  jet  of  hot  water  will  also  induce  a  similar  pain,  and  if  the  patient's 
eyes  be  shielded  no  difference  in  the  sensations  is  noted;  that  is, 
the  pulp  responds  to  thermal  stimuli,  hot  or  cold,  indifferently.  The 
organ  is  accustomed  to  variations  of  temperature  between  60°  and 
105°  to  110°  F.,  and  within  this  range,  in  a  condition  of  health,  takes 
no  apparent  cognizance  of  this  degree  of  change. 

With  a  decrease  in  the  amount  of  dentine  covering  the  pulp — i.  e., 
with  the  advance  of  caries — the  reaction  to  thermal  stimuli  increases 
in  promptness,  until,  when  the  pulp  is  nearly  exposed,  the  response  is 
immediate.  Succeeding  this  is  noted  prompt  response  to  lesser  degrees 
of  temperature  change,  until  the  pulp  comes  to  respond  immediately 
to  water  at  a  temperature  of  70°  F.,  or  thereabout,  and  slightly  over 
the  bodily  temperature,  102°  F.  Later,  another  feature  makes  its 
appearance;  instead  of  a  sharp  contraction  pain,  applications  of 
moderate  thermal  stimuli  are  followed  by  a  heavy,  throbbing  pain. 
Later,  similar  pains  occur  in  the  absence  of  tangible  external  sources 
of  irritation.  In  the  ordinary  sequence  of  events  intense  pain  is 
later  caused  by  hot  applications,  and  cold  applications  afford  relief. 

The  response  to  thermal  stimuli  may  pursue  the  opposite  course. 
The  normally  prompt  response  is  followed  by  delays  in  reaction,  until 
it  is  only  after  the  continued  application  of  cold  to  the  exterior  of  a 
tooth  that  a  paroxysm  of  pain  is  induced.  In  these  cases  there  follows 
after  a  long  time  an  increasing  response  to  heat,  as  in  the  former 
instance,  the  reaction  occurring  only  upon  decided  or  prolonged  heat 
stimuli.  Following  upon  the  period  of  increased  response  to  heat,  in 
both  cases  there  comes  a  period  of  quiescence,  in  which  there  is  no 
response  whatever  to  applications  of  intense  cold,  even  that  produced 
by  the  evaporation  of  a  spray  of  ethyl  or  methyl  chloride^ — i.  e.,  the 
sensory  function  of  the  pulp  is  paralyzed. 

These  are  the  available  subjective  evidences  of  the  anatomical  con- 
dition of  the  pulp;  while  they  indicate  with  a  degree  of  accuracy,  useful 
in  clinical  work,  the  alterations  in  the  pulp,  the  exact  relations  between 

1  American  System  of  Dentistry,  vol.  i. 


364  CONSTRUCTIVE  DISEASES. 

the  reactions  and  the  morbid  anatomy  of  the  organ  are  not  entirely 
clear.  In  the  light  of  personal  knowledge  it  is  assumed  that,  in  conse- 
quence of  the  loss  of  the  normal  protective  covering  of  the  pulp,  its 
sensory  and  perhaps  vasomotor  nerve  fibres  become  stimulated,  over- 
stimulated,  irritated,  then  paralyzed  by  thermal  stimuli  in  the  progress 
of  caries.  The  bloodvessels,  which  retained  their  tonus  up  to  a  certain 
point,  suffer  vasomotor  irritation;  next,  paralysis  leading  to  their  dila- 
tation and  to  the  throbbing  pain.  Later,  even  change  of  posture  is 
sufficient  to  cause  distention  of  the  paralyzed  vessels,  hence  pain  in 
resuming  the  reclining  position.  Stimulation  by  cold,  until  the  later 
stages,  causes  a  sharp,  continuous  pain,  ascribed  to  the  paroxysmal 
contraction  of  the  vessels;  although  unquestionably  specific,  sensory- 
nerve  reaction  is  involved.  In  the  stages  of  paralysis  heat  causes 
further  distention  of  the  vessels,  and,  if  adventitious  gases  be  present, 
causes  their  expansion  with  pressure  upon  nerve  filaments. 

The  decreasing  and  delayed  response  to  thermal  stimuli  must  be 
referred  to  two  sources:  first,  an  increase  in  the  non-conducting  cover- 
ing of  the  pulp — i.  e.,  a  lessening  of  the  amount  of  the  fluid  contents 
of  the  dentinal  tubuli  and  a  thickening  of  the  dentinal  walls,  which 
necessarily  implies  a  recession  of  the  pulp  from  its  normal  position; 
secondly,  to  degeneration  of  the  sensory-nerve  fibres  themselves;  and, 
thirdly,  changes  in  the  walls  of  or  about  the  bloodvessels,  which  check 
vasomotor  response  and  changes  in  the  calibre  of  the  vessels.  These 
two  classes  of  reactions  still  further  emphasize  the  division  of  pulp 
diseases  into  two  types,  the  acute  and  chronic;  the  first  class  of  reac- 
tion is  associated  with  the  acute  destructive  diseases;  the  second,  with 
the  chronic  constructive  but  degenerative  conditions. 

CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

The  constructive  diseases  of  the  dental  pulp  include  all  the  secondary 
dentine  formations,  tubular  calcification,  the  formation  of  pulp 
nodules,  and  calcareous  degeneration  of  the  pulp. 

Tubular  Calcification.  Definition.  By  tubular  calcification,  or,  to 
express  the  condition  more  accurately,  tubular  dentinification,  are 
meant  those  changes  that  occur  in  the  dentine  which  lead  to  an  oblit- 
eration of  the  dentinal  tubuli  by  constructive  changes  in  the  walls  of 
the  tubules. 

Causes  and  Occurrence.  The  apparent  cause  is  a  mild  degree  of 
irritation,  not  passing  the  stage  inducing  constructive  metamorphosis, 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP.         365 

and  apparently  caused  by  heightened  thermal  sensitivity  or  direct  irri- 
tation of  the  fibrillae.  It  occurs  in  the  course  of  mechanical  abrasion 
and  erosion  of  the  teeth,  under  metallic  fillings,  and  probably  a  modi- 
fication of  the  process  precedes  the  slow  invasion  of  dental  caries.  It 
occurs  in  some  degree  as  a  normal  vital  change  due  to  age,  and  is  com- 
mon in  persons  who  are  victims  of  the  gouty  or  rheumatic  diathesis. 

Pathology.  The  fibrilla  is  lessened  in  diameter  as  the  lumen  of  the 
tubule  becomes  smaller.  There  is  sometimes  an  increased,  but  more 
often  a  lessened,  sensitivity  of  the  dentine. 

Other  phases  of  the  condition  are  discussed  under  transparency  of 
the  dentine,  to  which  the  disease  corresponds.     (See  p.  309.) 

The  altered  dentine  becomes  translucent,  acquiring  a  horn-like 
appearance. 

Tubular  calcification  is,  for  the  most  part,  to  be  regarded  in  the 
light  of  an  effect  due  to  a  physiological  process.  In  so  far  as  the 
disease  is  confined  to  the  dentine,  it  may  be  regarded  as  a  physio- 
logical barrier  erected  against  the  progress  of  caries,  erosion,  or  abrasion, 
threatening  the  invasion  of  the  pulp.  While  it  delays  the  disintegra- 
tion of  the  tissue,  it  does  not  prevent  it.  In  the  cases  due  to  age  or 
the  irritants  produced  by  gout,  it  is  probably  a  local  expression  of  a 
general  sclerotic  change,  the  intercellular  substance  (tubule  wall)  being 
formed  at  the  expense  of  the  cellular  (fibrilla).  In  senility  the  change 
in  the  dentine  may  cause  the  teeth  to  be  almost  transparent.  It 
requires  no  treatment. 

Secondary  Dentine.  Definition.  By  secondary  dentine  is  meant  a 
deposit  of  dentine  upon  the  wall  of  the  pulp  chamber,  as  the  result 
of  pulp  stimulation  after  the  pulp  has  enjoyed  a  physiological  period 
of  rest  from  dentine  formation.    It  is  always  attached  to  the  dentine. 

Causes.  The  cause  of  formation  of  secondary  dentine  is  a  stim- 
ulation of  the  pulp  to  increased  functional  activity.  This  stimulus 
may  be  provided  by  any  constant  irritation  of  the  dentinal  fibrillse, 
as,  for  example,  when  exposed  at  necks  of  teeth,  upon  abraded  or 
eroded  surfaces,  or  within  cavities  of  decay.  The  presence  of  metallic 
fillings  conductive  of  thermal  changes  may  provide  the  necessary 
stimulus.  Gold  crowns  upon  ground-down  crowns  of  vital  teeth  have 
a  similar  effect.  The  slightly  irritative  effects  of  oxychloride  of  zinc 
often  produce  much  secondary  dentine.  A  pulp  capping  may  provide 
the  stimulus  and  new  dentine  fill  the  orifice  of  exposure. 

Absolute  exposure  without  treatment  has  been  recorrded  as  pro- 
ductive of  secondary  dentine.     In  two  cases  described  by  Charles 


366 


CONSTRUCTIVE  DISEASES. 


Tomes,  pulps  widely  exposed  by  fracture  of  crowns  during  extraction 
covered  themselves  completely  in.     The  histological  record  as  seen 


Fig.  338. 


Fig.  339. 


Secondary  dentine 
formed  after  exposure 
of  pulp  by  fracture  dur- 
ing extraction.  (Tomes.) 

Fig.  340. 


Bicuspid  in  which  a 
formation  of  secondary 
dentine  has  failed  to  ob- 
viate perforation  of  the 
pulp  cavity  by  resorp- 
tion.   (Tomes.) 


Harding's  case  of  united  fracture.     The  uniting  material  is  of  coarse 
osseous  structure  with  numerous  lacunal  spaces.     (Tomes.) 


Fig.  341. 


in  the  photomicrograph  demonstrated  that  a  plastic  exudation  was 
first  exuded,  which  later  calcified  as  an  amorphous  mass. 

Next  an  irregular  lamina  was  formed,  and, 
lastly,  dentine  containing  tubules.  It  is  to  be 
inferred  that  both  the  pulp  and  its  odontoblasts 
may  take  part  in  the  process  (Fig.  338). 

I  have  seen  one  case  in  which  a  wide  expo- 
sure had  been  covered  in  sufiiciently  to  enable 
me  to  gently  indent  the  covering,  which  was 
convex,  with  a  ball  burnisher.  Upon  removal 
of  the  instrument  it  resumed  its  original  shape 
owing  to  its  elasticity.  The  periphery  of  the 
original  exposure  was  clearly  defined  (Fig.  341). 
Age  seems  to  be  a  cause  of  general  secondary 
dentine  formation,  but  no  doubt  certain  forms  of  irritation  are  intro- 
duced competent  to  produce  the  changes.     At  times  reflex  irritation 


Elastic  layer  of  calcific 
m.aterial  formed  over  an 
exposed  pulp.  From  a 
case. 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


367 


seems  to  be  a  competent  cause,  as  in  cases  of  partial  abrasion  the 
unworn  teeth  may  be  affected  in  equal  degree  with  the  worn  ones. 

Pathology  and  Morbid  Anatomy.  The  formation  is  usually  noted 
opposite  to  some  area  of  injury  and  may  be  distinguished  from  normal 
dentine  by  its  translucency,  or  sometimes  by  its  color,  which  may  be 
a  light  brown.  The  deposit  may  be  of  fairly  regular  or  irregular 
distribution,  and  even  tumors  attached  to  the  dentine  have  been 
described  (Figs.  340  and  344). 


Fig.  342. 


Fig.  343. 


Fig.  342. — Secondary  dentine  filling  the  pulp  chamber  in  a  case  of  abrasion  of  a  cuspid  tooth: 
o,  portion  lost  by  abrasion;  c.  abraded  surface;  d,  secondary  dentine,  filling  a  portion  of  the  pulp 
chamber,  and  acting  as  a  protection  to  the  pulp;  e,  slender  point  of  the  pulp;  irregular  deposits 
are  seen  on  the  walls  of  the  pulp  chamber,  as  at/;  g,  cylindrical  calcifications  in  the  root  portion 
of  the  pulp  chamber. 

Fig.  343. — Secondary  dentine  from  the  same  specimen  as  Fig.  342,  magnified  sufficiently  to 
show  the  difference  in  -primary  and  secondary  tissue:  a,  abraded  surface  crown;  6,  secondary 
dentine;  c,  primary  dentine;  d,  junction  of  primary  with  secondary  dentine;  e,  remains  of  pulp 
tissue;  /,  small  oval  masses  of  calcific  material.     (Black.) 

Black  has  shown  that  in  the  deposits  against  normal  dentine  the 
first-formed  portion  contains  an  almost  normal  number  of  tubules, 
but  their  direction  is  sharply  changed.  As  the  deposits  become  thicker, 
the  tubules  become  fewer  and  finally  the  dentine  becomes  amorphous 
in  character  (Fig.  347). 

Black  relates  these  appearances  with  the  gradual  atrophy  and  dis- 
appearance of  the  odontoblasts. 


368 


CONSTRUCTIVE  DISEASES. 


Hopewell-Smith,  treating  of  secondary  dentine  under  the  title  of 
"Adventitious  Dentine,"  mentions  several  varieties :  (1)  Fibrillar,  or  that 
containing  tube-like  markings  finer  and  less  regular  than  in  normal 
dentine.  This  would  correspond  to  that  in  Fig.  344,  h.  (2)  Areolar, 
that  containing  interglobular  spaces  formed  by  the  non-union  of  calco- 
spherites.  (3)  Cellular,  or  that  in  which  the  connective-tissue  cells 
of  the  pulp  remain  encapsuled  in  the  calcifying  matrix.  (4)  Laminar, 
in  which  laminated   spherites   appear    (Fig.  344,  c).     (5)   Hyaline, 

Fig.  344. 


Dentinal  tumor  -n-ithin  pulp  chamber:  A,  diagram  of  the  tooth,  with  dotted  line  showing  the 
position  of  the  section  B.  In  B  the  pulp  chamber  is  shown  in  section,  nearly  natural  size,  show- 
ing the  tumor  within.  Cis  an  illustration  of  the  tissue  of  the  tumor;  a,  a,  the  primary  dentine; 
b,  irregular  tubules  connecting  the  new  growth  with  the  primary  dentine — most  of  these  are  very 
dark  and  irregular;  c,  a  calcospherite  included  in  the  mass;  d,  apparently  a  bloodvessel  calcified; 
e,  calcified  tissue;  /,  a  finely  granular  mass;  g,  a  spur  of  very  transparent  dentine.  Dentinal 
tubules  appear  at  h,  h.     (Black.) 


having  a  granular  or  ground-glass-like  appearance  (the  amorphous 
substance  of  Black).     (Fig.  344,  /.) 

He  regards  the  adventitious  dentines  as  formed  by  pulp  cells  rather 
than  by  the  odontoblasts. 

In  these  cases  the  pulp  deposits  calcoglobulin  against  the  dentine. 
Apparently  in  some  of  Black's  cases  the  calcoglobulin  was  deposited 
about  pre-existing  fibrillae  which  continued  to  persist  in  the  new- 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


369 


formation,  while  in  Tomes'  cases  the  pulps  were  compelled  to  calcify 
a  plastic  exudation  as  a  sort  of  basis  for  the  beginning  of  tubule 
formation.  Black  has  shown  that  in  abrasion  the  deposit  is  more 
regular  than  in  caries,  without  doubt  due  to  the  fact  that  the  thermal 
irritation  in  caries  is  more  irregular  than  the  irritation  of  the  fibrillse 
by  abrasion. 

The  entire  crown  may  be  removed  by  abrasion  and  yet  the  pulp 
be  protected.  In  some  cases  the  protective  action  ceases  and  the 
pulp  becomes  closely  approached  or  exposed  (Fig.  256). 

The  mode  of  deposition  upon  the  sides  of  the  canal  in  abrasion, 
shown  by  Fig.  347,  is  quite  characteristic. 

Fig.  345. 


Fig.  345. — Illustration  of  the  narrowing  of  the  pulp  chamber  in  a  molar  (superior)  by  the 
deposit  of  secondary  dentine  resulting  from  abrasion,  showing  the  portions  of  the  chamber  in 
which  the  deposit  usually  occurs.  The  light-shaded  portion  (6)  shows  the  original  dimensions  of 
the  chamber,  which,  in  this  instance,  seem  to  have  been  pretty  large;  a,  a  point  of  deep  abrasion; 
c,  c,  remaining  pulp  chamber,  which  is  mostly  filled  with  irregular  masses;  d,  one  of  the  root 
canals.  It  will  be  observed  that  the  narrowing  of  the  root  canal  is  within  the  original  pulp 
chamber.     (Black.) 

Fig.  346. —P.-D.,  primary  dentine;  S.D.,  secondary  dentine;  F,  pulp  chamber;  D,  nodules. 

Deposits  in  canals  may  occur,  lessening  their  lumen  and  increasing 
the  difficulty  of  canal  exploration  (Fig.  349). 

"  Secondary  growths  in  cases  of  abrasion  are  not  confined  alone  to 
the  abraded  teeth,  but  other  teeth  which  have  escaped  wear  may  be 
affected  in  equal  degree.  In  all  of  these  cases  there  is  direct  evidence 
that  the  odontoblastic  layer  has  been  stimulated  to  increased  activity 
and  produced  the  regular  secondary  deposition."  ^ 

Secondary  dentine  is  often  accompanied  by  other  constructive 
changes  in  the  pulp — i.  e.,  pulp  nodules  and  calcareous  degeneration 
(Figs.  346  and  352). 

Miller  has  shown  that  dentine  resorption    by  the  pulp  may  be 


'  Black,  American  System  of  Dentistry,  vol.  i. 
24 


370 


CONSTRUCTIVE  DISEASES. 


repaired  by  a  new  deposit  of  secondary  dentine,  which  Hopewell- 
Smith  has  shown  to  be  of  the  nature  of  cementum  (Fig.  365). 

Tomes^  describes  and  illustrates  a  peculiar  case  of  united  fracture 
occurring  in  the  practice  of  Mr.  Harding.  In  an  incisor  an  oblique 
fracture  occurred  which  entirely  separated  the  fractured  segment, 
yet  a  plastic  exudate  from  the  pulp  occurred  which,  when  calcified, 
attached  it  to  the  fixed  portion  of  the  tooth.  The  new-formation 
did  not  resemble  dentine  (Fig.  339). 


Fig.  347. 


Calcification,  or  deposit  of  secondary  dentine,  resulting  from  caries  of  an  incisor:  A,  diagram 
of  section  of  incisor,  showing  caries  at  a,  and  secondary  dentine  at  b.  B,  illustration  magni- 
fied 200  diameters,  to  show  the  tissue  of  the  secondary  dentine:  a,  pulp  chamber;  6,  b,  secondary 
dentine;  c,  primary  dentine.  It -^^-ill  be  noticed  that  the  dentinal  tubes  in  the  secondary  dentine 
gradually  disappear,  giving  place  to  a  clear  calcification.      (Black.) 

Fig.  273  illustrates  a  case  of  repair  of  an  incisor  fractured  at  a 
point  well  up  beneath  the  gum,  a  condition  reasonably  ensuring 
asepsis.    A  firm  reattachment  occurred.     (See  Fig.  266.) 

Kirk^  records  a  case  of  immediate  replantation  in  early  life,  followed 
in  old  age  by  root  resorption.  The  tooth  when  extracted  contained 
secondary  dentine  which  could  only  have  formed  as  the  result  of  a 
reattachment  of  the  pulp. 

W.  H.  Trueman^  reported  that  hypersensitive  dentine  was  noted 
some  years  after  a  replantation  under  similar  conditions. 


1  Dental  Surgery, 
s  Ibid. 


-  Proceedings  of  the  Academy  of  Stomatology,  1902. 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


371 


Osteodentine.  Tomes  states  that  secondary  dentinal  deposits  may 
assume  the  character  of  osteodentine,  a  form  of  dentine  found  in  the 
teeth  of  some  animals,  in  which  the  tissue  presents  combined  char- 
acteristics of  both  bone  and  dentine.  He  cites  the  example  also  that 
elephants'  tusks  are  frequently  repaired  with  osteodentine  after  injury. 
The  specimen  illustrated  (Fig.  348)  was  taken  from  a  case  in  which 
the  coronal  portion  of  the  pulp  chamber  was  almost  obliterated  by  a 
deposit  of  secondary  dentine.  Probably  some  of  the  pulp  cells  have 
taken    on    the    characteristics    of    osteoblasts.     Tissue    resembling 

Fig.  348. 


Osteodentine:  A,  outline  of  incisor,  showing  a  narrowing  of  the  root  canal  at  &  by  a  deposit 
of  osteodentine.  B,  illustration  of  the  tissue:  a,  primary  dentine;  6,  line  of  the  beginning  of  a 
growth  of  secondary  dentine;  c,  secondary  dentine;  d,  layer  of  granular  matter;  e,  osteodentine; 
this  has  the  lacunae  at  g  and  dentinal  tubes  at  k ;  f  seems  to  be  the  surface  of  the  osseous 
deposit;  i,  irregular  crystalline  deposits;  h,  the  pulp  chamber.     X  350.     (Black.) 


cementum  seems  to  be  frequently  found  as  a  tissue  of  repair 
(Fig.  365). 

Results  of  Secondary  Dentine.  The  formation  of  large  masses  of 
secondary  dentine  unquestionably  brings  about  a  degenerative  con- 
dition of  the  pulp  which  may  become  a  cause  of  neuralgia.  The  pulp 
may  die  and,  becoming  infected,  may  produce  pericemental  irritation. 
In  one  case  seen  the  secondary  deposit  in  the  pulp  chamber  had 
separated  the  canal  filaments  of  the  pulp  of  a  multirooted  tooth  into 
independent  pulps,  one  of  which  was  dead  and  the  others  alive  and 
undergoing  degeneration.  The  specific  symptoms  were  those  of  peri- 
cementitis— i.  e.,  elongation  and  tenderness  to  percussion. 

In  another  case  of  a  first  upper  bicuspid  the  lingual  filament  was 


372  CONSTRUCTIVE  DISEASES. 

perfectly  covered  in  and  apparently  vital.  The  buccal  filament, 
likewise  enclosed  and  isolated,  contained  an  abscess  within  the  pulp. 

The  symptoms  complained  of,  however,  were  those  of  acute  peri- 
cemental irritation,  simulating  incipient  septic  apical  pericementitis 
(Fig.  375). 

It  has  been  shown  by  Hopewell-Smith  that  micro-organisms  may 
enter  the  pulp  by  way  of  the  spaces  or  tubes  in  adventitious  dentine. 
In  Burchard's  case  a  molar  containing  a  deep  cavity  filled  with  zinc 
phosphate  gave  vague  pain,  finally  referred  to  the  tooth,  which 
responded  only  faintly  to  hot  applications  and  not  at  all  to  cold  ones. 
Secondary  dentine  was  found  complicated  by  calcareous  degeneration 
— i.  e.,  a  degenerated  pulp  was  present. 

In  certain  cases  a  deposit  extends  well  into  a  canal,  totally  obliter- 
ating it  for  much  of  its  length.  Unless  symptoms  be  present  it  may 
ordinarily  be  left.  In  such  cases  thermal  tests  for  pulp  vitality  seem 
often  inconclusive.  The  electric  current  should  be  a  more  satisfactory 
means  of  diagnosis,  provided  the  dentine  be  moist.  (See  Dry  Gan- 
grene.) 

Treatment.  Secondary  dentine  which  has  been  regularly  deposited, 
and  particularly  in  the  canals  of  anterior  teeth,  calls  for  no  treatment. 
Should,  however,  great  hypersensitivity  of  the  dentine  and  pulp,  or 
pulp  disease,  be  e\ddent  or  inferred  from  symptoms,  the  pulp  should 
be  removed.  This  may  involve  a  search  of  some  difficulty  and  necessi- 
tate the  removal  of  much  dentine.  The  canals  may  be  much  con- 
stricted, especially  at  that  portion  nearest  the  pulp  chamber.  The 
condition  may  be  more  or  less  complicated  by  the  presence  of  pulp 
nodules  or  calcific  degenerations  in  addition  to  the  secondary  dentine. 

Pulp  Nodules.  Definition.  Pulp  nodules  (pulp  stones,  nodular 
calcifications)  are  masses  of  more  or  less  translucent,  calcific  material, 
apparently  the  result  of  secretion,  having  a  fairly  definite  histological 
structure  differing  from  that  of  dentine,  and  occupying  a  position 
within  the  pulp  substance.  They  are  rarely  fused  with  the  dentinal 
walls  of  the  pulp  chamber,  and  then  are  included  by  formation  of 
secondary  dentine. 

Occurrence.  While  these  growths  may  occupy  the  pulp  chambers 
of  teeth  in  which  the  pulp  has  been  the  seat  of  direct  irritation,  their 
occurrence  is  by  no  means  confined  to  such  teeth.  They  are  found  not 
only  in  teeth  which  have  suffered  abrasion,  erosion,  and  slowly  progress- 
ing caries,  but,  as  pointed  out  by  Black,  they  may,  and  frequently  do, 
form  in  other  teeth  of  the  same  denture  which  are  not  directly  involved 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


373 


in  the  irritation.  This  investigator  notes  that  irritation  of  the  pulp 
of  one  tooth  of  a  denture  very  frequently  causes  a  general  hyper- 
eesthesia  of  the  pulps  of  all  of  the  teeth.  This  is  particularly  notable 
in  the  type  of  persons  classed  as  neuralgic.  It  is  also  common  in 
persons  of  the  gouty  diathesis.    It  should  be  remarked  that  a  general 

Fig.  349. 


A  pulp  nodule  fused  to  the  parietes  of  a  pulp  cavity.     Prepared  by  grinding.    PX,  pulp  nodule; 
J),  dentine  of  the  tooth.     X  15.     From  section  by  J.  F.  Colyer.     (HopeweU-Smith.) 


pulp  hypersesthesia  is  frequently  the  precursor  of  an  acute  outbreak 
of  gout  in  such  persons.  Nodules  are  found  much  more  frequently 
in  the  teeth  of  middle-aged  persons  than  in  those  of  youth,  although 
they  may  be  present  as  early  as  the  fifteenth  year.  They  occur  more 
frequently  multiple  than  single.  Some  of  the  larger  nodules  are 
evidently  formed  by  the  coalescence  of  smaller  ones. 


374 


CONSTRUCTIVE  DISEASES. 


Pathology  and  Morbid  Anatomy.  The  structure  of  pulp  nodules  does 
not  resemble  that  of  dentine;  they  possess  about  the  same  degree  of 
translucency  and  hardness.    Outwardly  they  may  assume  almost  any 


Fig.  3.50. 


Section'of  a  pulp  nodule,  showing  many  calcospherites,  as  pointed  out  by  a,  a.     (Black.) 

form;  they  range  in  size  from  minute  bodies  to  a  size  sufficient  to 
almost  obliterate  the  pulp  (Figs.  346  and  352). 

A  section  of  a  nodule  exhibits  the  presence  of  a  number  of  concen- 
trically laminated    bodies,  recognizable  as  hardened   calcospherites. 


Fig.  3.51. 


Deposit  of  calcoglobulin  within  the  tissues  of  an  inflamed  pulp.      (Black.) 

Black  found  them  to  rarely  make  up  any  considerable  portion  of  the 
bulk  of  the  nodule.  The  remainder  of  the  nodule  is  made  up  of 
structureless  material  which  may  contain  a  few  fine  tubes. 

He  also  found  deposits  in  the  pulp  which  throw  light  upon  the 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


375 


possible  origin  of  nodules  in  some  cases,  and  to  some  extent  upon 
the  conditions  under  which  they  may  be  formed.  In  the  pulp  of 
a  second  molar  of  a  girl  aged  fifteen,  in  which  there  had  been 
decided  subjective  evidences  of  pulpitis  recurring  at  intervals  for  a 
period  of  two  months,  he  found  a  mass  representing  a  pulp  nodule  in 
its  soft  state.  "About  one-half  of  the  coronal  portion  of  the  pulp  was 
involved  in  the  inflammation;  lying  a  little  inside  of  the  layer  of  odonto- 
blasts were  several  masses  similar  to  Fig.  351,  having  globular  forms 


CalcificatioD  of  the  dental  pulp.  At  A  is  shown  the  outline  of  a  lower  molar  with  a  canity 
at  b.  The  pulp  chamber  is  much  reduced  in  size  and  filled  with  calcific  material,  as  shown 
in  B.  a,  a,  large  granular  mass  of  calcific  material,  which  is  very  transparent  but  finely 
granular.  A  very  few  irregular  lines  are  seen  in  the  centre,  which  sHghtly  resemble  dentinal 
tubes;  b,  an  erratic  growth  of  irregularly  formed  and  unusually  transparent  dentine;  e.  hue  of 
the  growth  of  dentine  from  the  floor  of  the  pulp  chamber:  the  growth  from  other  directions 
is  so  perfectly  regular  as  to  leave  no  markings;  d,  margin  of  the  canity  of  decay;  e,  a  btmdle 
of  cylindrical  forms  of  calcific  material  extending  down  into  the  root  canal.  These  extended 
to  the  apex  of  the  root.-    (Black.) 

in  their  mass  or  attached  to  their  margins.  The  globular  bodies 
present  the  laminated  appearance  of  calcospherites."  These  masses 
may  in  all  probability  be  interpreted  as  intermediate  products  in  the 
formation  of  nodules;  they  have  not  yet  become  calcified. 

A  small  nodule  may  be  made  up  of  laminated,  structureless  material, 
the  laminee  being  arranged  about  a  central  nucleus,  the  nature  of 
■which  is  not  clear,  but  may  possibly  be  calcified  dead  cells  (Fig.  353). 

The  conditions  of  calcification  of  nodules  are  not  definitely  known. 


376 


CONSTRUCTIVE  DISEASES. 


Hopewell-Smith  considers  that  they  are  deposited  by  the  pulp  cells  as 
a  secretion  about  themselves,  and  that  the  cells  are  later  obliterated 
or  may  persist  iti  situ  (Fig.  354).  He  also  describes  and  illustrates 
a  case  of  a  nodule  which  had  within  it  a  pulp  cavity  containing  pulp 
tissue. 

Pulp  nodules  occur,  as  a  rule,  in  the  better  grades  of  teeth  which  show 
constructive  tendencies  upon  the  part  of  the  pulp. 

It  is  possible  that  in  these  pulps  the  pulp  cells  under  conditions  of 
irritation  secrete  calcoglobulin,  which  in  part  is  developed  into  spherites 
and  in  part  remains  without  definite  histological  characteristics.  The 
masses  are  probably  calcified  after  their  deposition.  Whatever  the 
origin  of  the  masses — by  cell  secretion  or  otherwise — the  histological 

Fig.  353. 


A  pulp  nodule  isolated  from  the  pulp.  Shows  its  central  nuclear  formation  and  its  concentric 
lamination.  Prepared  by  grinding.  X  50.  From  collection  of  G.  W.  Watson  (Hopewell- 
Smith.) 

record  indicates  a  gradual  increase  in  the  size  of  the  deposit.  Pressure 
upon  the  nerves  results  in  irritation.  Pulp  nodules  are  usually  found 
in  the  coronal  portion  of  the  pulp,  but  sometimes  exist  in  the  root 
portions,  either  free  or  embedded  in  secondary  dentine.  If  they 
obstruct  the  lumen  of  the  canal  they  cause  interference  with  the 
circulation  and  nerve  tissue  and  may  produce  great  pain. 

Symptoms.  ^Multiple  nodules  may  exist  in  a  dental  pulp  and  give 
rise  to  no  evident  s\T2iptoms  whatever,  as  is  shown  by  their  presence 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP.         377 


in  extracted  teeth,  many  of  them  free  from  caries,  and  in  which  there 
was  no  history  of  pain.  On  the  contrary,  the  pulp  of  a  tooth  may 
be  the  seat  of  intractable  pain  without  a  depth  of  carious  invasion 
which  would  lead  to  the  inference  of  acute  pulp  disease;  and  relief 
only  be  secured  through  divitalization  of  the  pulp,  which  upon  exami- 
nation may  reveal  a  small  pulp  nodule. 

The  symptoms  attendant  upon  the  presence  of  nodules,  so  far  as 
they  can  be  made  out,  appear  to  be  of  two  types — those  associated  with 
small  and  those  with  extensive  deposits.  Reflex  pain  is  the  common 
associate  of  both. 

Fig.  354. 


FN 


3IN 


The  formation  of  the  pulp  nodule.  Prepared  by  Mr.  Hopewell-Smith's  process.  PiV,  pulp 
nodules;  M  JV,  medullated  nerve  bundles;  P,  pulp  tissue;  C,  capillary.  X  2S0.  (Hopewell- 
Smith.) 

Small  Deposits.  While  it  is  true  that  pulp  nodules  exist  in  appar- 
ently sound  teeth  without  inducing  pain,  yet  the  pulps  of  teeth  con- 
taining them  become  excessively  hypersesthetic  under  what  are  ordi- 
narily mild  sources  of  irritation.  This  is  manifested,  first,  through 
the  contents  of  the  dentinal  tubuli;  the  dentine  becomes  exquisitely 
sensitive,  and  cool  water  directed  into  a  shallow  cavity  produces  a 
paroxysmal  and  excruciatingly  painful  response  from  the  pulp.  In  the 
absence  of  direct,  extraneous  irritation  of  the  pulp,  the  dental  symp- 
toms may  be  absent,  but  a  persistent  neuralgia  may  be  located  at 
some  distant  point.  Pain  in  the  ear  is  a  frequent  symptom.  Occasion- 
ally an  obstinate  scalp  neuralgia,  with  the  existence  of  a  hypersesthetic 


378 


CONSTRUCTIVE  DISEASES. 


spot,  appears.  Pain  in  the  eye,  with  tenderness  over  the  supra-orbital 
foramen,  is  also  common.  Guilford^  has  reported  a  case  of  tic  doulou- 
reux of  two  years'  standing,  the  result  of  pulp  nodules.  The  pain  may 
be  recurrent  or  persistent.  If,  in  the  absence  of  a  more  probable  expla- 
nation of  the  pain,  a  pulp  nodule  be  suspected,  and  arsenical  applica- 
tions be  made  to  devitalize  the  pulp,  it  is  found  that  not  only  is  intense 
pain  caused,  but  examination  after  from  forty-eight  to  seventy-two 
hours  shows  the  pulp  to  be  still  vital  and  hypersensitive;  and,  in  order 
to  effect  its  destruction,  repeated  applications  and  large  doses  of  arsenic 
must  be  used.  Cocaine  introduced  by  cataphoresis  is  also  apt  to  be 
slow  in  action. 

Large  Deposits.  In  extensive  deposits  of  pulp  nodules  the  dentine 
may  be  almost  devoid  of  sensation,  and  applications  of  heat  or  cold, 
even  in  large  cavities,  may  be  followed  by  delayed  and  faint  pulp 
response.     Such  cases,  however,  commonly  give  a  history  of  reflex 


Fig.  355. 


Fig.  356. 


Pulp  nodules  in  the  radicular  and  coronal  portions  of  the  canal.      (Skiagraphs  by  Price.-') 

neuralgia  and  vague  dental  pains  extending  over  a  period,  it  may  be, 
of  years.    With  some  large  deposit  the  pain  may  be  exquisite. 

Diagnosis.  Their  diagnosis  by  means  of  the  x-ray  is  positive  (Figs. 
355'and  356),  but  their  diagnosis  by  symptoms  may  only  be  inferential 
and  confirmation  be  lacking  until  after  devitalization  of  the  pulp  and 
the  finding  of  the  pulp  nodules  in  its  substance. 

The  tardy  action  of  arsenic  is  also  observed  in  the  cases  of  large 
deposits,  it  being  frequently  necessary  to  devitalize  the  pulp  piece- 
meal, and  sometimes  the  arsenic  will  hardly  be  tolerated  at  all. 

Treatment.  Pulps  inferred  or  shown  by  x-ray  to  contain  nodules 
should  be  removed.  If  the  cataphoric  apparatus  be  at  hand  it  may 
be  used  to  benumb  the  pulp  by  cocaine;  at  least,  sufficiently  for  the 
removal  of  the  nodule.  If  desired,  the  remainder  of  the  pulp  may  be 
anaesthetized    by  cataphoresis    or    cocaine  pressure    an(3esthesia   and 


1  Private  communication. 


-  Items  of  Interest,  1901. 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP.  379 

removed.  The  bloodletting  attendant  upon  removal  of  the  bulb  of 
the  pulp  usually  permits  an  arsenical  application  for  devitalization 
of  the  remainder  of  the  pulp  to  be  painlessly  made,  but  this  is  not 
always  the  case. 

The  same  result  may  be  attained  by  drilling  open  the  pulp  cavity 
while  the  patient  is  under  the  influence  of  nitrous  oxide  gas. 

At  times  arsenic  may  be  applied  to  the  pulpal  wall  of  the  cavity, 
if  one  exist,  or  in  a  specially  prepared  pocket,  without  production  of 
painful  reaction. 

After  forty-eight  hours  a  portion  of  dentine  is  to  be  removed  and 
a  stronger  application  made.  When  the  pulp  is  closely  approached, 
the  arsenic  is  to  be  left  a  week  or  longer  in  position,  when,  as  a  rule, 
the  nodule  may  be  removed.  Another  application  may  then  be  left 
in  position  for  a  week  or  longer  to  ensure  devitalization. 

If,  after  devitalization,  the  nodule  or  calcific  degeneration  be  found 
as  a  spicular  deposit  in  the  mouth  of  the  canal,  it  may  usually  be 
removed  by  teasing  it  from  side  to  side,  first  soaking  the  part  with 
a  sodium  dioxide  solution,  or  50  per  cent,  sulphuric  acid,  which  quickly 
destroys  the  organic  matter  of  the  pulp. 

Pericemental  reactions  are  quite  apt  to  follow  the  removal  of  such 
pulps.  This  result  is  best  obviated  by  awaiting  the  thorough  death 
of  the  pulp  filaments  before  attempting  their  removal. 

If  such  reaction  arise,  sedatives,  such  as  tincture  of  aconite  plus 
cocaine,  are  to  be  applied  on  cotton  as  root-canal  dressings,  and 
counterirritants  are  to  be  applied  to  the  gum.  (See  Aseptic  Apical 
Pericementitis.) 

Calcific  Degeneration  of  the  Pulp.  By  a  calcific  degeneration  is 
meant  the  infiltration  of  inorganic  matter  derived  from  the  lymph  into 
tissue  which  is  dead  or  undergoing  degeneration.  It  occurs  in  any 
part  of  the  body  in  which  the  necessary  conditions  are  present.  (See 
p.  66.) 

Causes  and  Pathology.  The  conditions  apparently  necessary  for  the 
production  of  calcific  degeneration  are  those  which  occur  in  a  semi- 
stagnant  blood  current.  An  acid  reaction  occurs  owing  to  the  presence 
of  an  excess  of  carbon  dioxide.  The  albuminous  matter  of  the  tissue 
undergoes  degenerative  changes  owing  to  the  faulty  nutritive  supply 
and  waste  removal. 

Probably  some  cells  die.  They  or  their  constituents  have  some 
aflfinity  for  inorganic  salts  which  are  taken  up  from  the  lymph.  Thus 
gradually  the  tissue  becomes  infiltrated. 


380 


CONSTRUCTIVE  DISEASES. 


Those  causes  which  produce  a  sufficient  degeneration  of  pulp  tissue 
to  induce  the  above  process  are:  (1)  the  pulp  exhaustion  due  to  the 
formation  of  secondary  dentine  or  pulp  nodules;  (2)  continued  h}^er- 
semia  or  chronic  inflammation  in  which  venous  hyperemia  plays  a 
part. 

Pathology  and  Morbid  Anatomy.  The  calcic  material,  unlike  the 
cases  of  nodular  calcification,  encloses  the  anatomical  elements  of  a 
pulp  in  process  of  degeneration  in  a  mass  produced  by  deposition, 
not  secretion.  In  the  root  portions  of  pulps  in  which  fibrous  elements 
have  become  pronounced  the  calcification  may  be  tubular  or  cylindrical 
in  character,  the  nature  of  the  calcareous  masses  being  apparently  a 
deposition  about  and  along  the  fibres  (Fig.  357). 

Fig.  357. 


A,  outline  of  a  lower  molar,  -with  a  large  carious  cavity  at  a;  b,  pulp  chamber;  the  shaded 
portion,  c,  was  occupied  by  cylindrical  calcifications.  B,  cylindrical  calcifications.  X  100. 
(Black.) 

The  pulps  are,  of  course,  living.  There  is  a  comparative  absence 
of  cellular  elements  in  the  pulp — i.  e.,  they  have  atrophied,  degen- 
erated, and  been  absorbed.  Upon  optical  examination  the  masses  are 
seen  to  be  opaque,  are  brittle,  and  decidedly  unlike  pulp  nodules  in 
form. 

Anothe;  e\4dence  of  the  cellular  degeneration  is  seen  in  the  great 
ease  with  which  such  pulps  are  removed  after  devitalization,  even 
the  most  minute  apical  portions  freely  coming  away  upon  slightly 
catching  a  hook  in  the  pulp. 

The  usual  odontoblastic  attachment  to  the  dentine  is  not  present. 
When  extracted  these  pulps  have  a  granular  feel  to  the  fingers,  and 
when  dry  are  quite  stiff  (Fig.  358). 

Symptoms.  Degenerations  of  the  pulp,  as  a  rule,  present  symptoms 
of  reflex  pain,  vaguely  referred  to  other  parts.  The  response  to  hot 
applications  is  usually  greater  than  that  to  cold  ones,  and  both  are 


CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP.         381 

delayed — i.  e.,  five  seconds  or  more  may  elapse  before  pain  follows 

a  severe  test  like  the  intensely  cold  spray  of  ethyl  chloride  or  a  hot 

burnisher  or  blast  of  hot  air.    At  times  with  an 

open  pulp  chamber  the  symptoms  of  chronic 

pulp  inflammation  are  obtained.     There  may 

be  a  painful  reaction  to  arsenic  applied  to  the 

pulp. 

Diagnosis  and  Treatment.  The  a:-ray  should 
afford  a  positive  diagnosis,  but  in  its  absence 
the  diagnosis,  apart  from  the  inference  from 
the  symptoms,  is  a  post-mortem  one.    In  cases      Lingual  filament  of  puip  of 

,         .  „  .  I'll  .an  upper  molar,  broken  in  ex- 

warrantmg  the  mterterence,  m  which  there  is  traction.  The  rigidity  of  the 
a  delayed  response  to  intense   thermal  tests  filament  was  due  to  the  pres- 

•^  ^  _  ence  of  calcific  granules. 

applied  to  a  filling  or  a  clean  pulpal  wall,  the 

dentine  over  the  pulp  should  be  removed  and  the  pulp  devitalized. 
Upon  removal  of  the  pulp  it  may  be  found  to  contain  one  or  more 
large  or  many  granular  masses. 

Fig.  358  illustrates  a  case  discovered  upon  fracture  of  a  molar 
during  the  operation  of  extraction.  In  another  case  the  pulp  was 
slightly  bendable  when  extracted,  but  after  drying  for  a  half-hour 
became  at  its  apical  end  of  needle-like  sharpness  and  stiffness.  It 
was  filled  with  calcific  granules. 

The  constructive  diseases  of  the  pulp  are  an  evidence  of  an  attempt 
upon  the  part  of  the  pulp  to  protect  itself;  but  with  the  exception, 
perhaps,  of  a  very  regularly  deposited  secondary  dentine  the  effects 
react  upon  the  pulp  itself,  causing  its  destruction.  To  what  extent, 
therefore,  secondary  dentine  is  beneficial  is  an  open  question. 

Evidences  of  constructive  action  upon  the  part  of  the  pulp  may 
occasionally  be  noted  in  the  temporary  teeth — e.  g.,  secondary  dentine 
following  deep  abrasion. 

There  do  not  seem  to  be  any  observations  as  to  the  formation  of 
nodules  or  calcific  degenerations  in  the  pulps  of  temporary  teeth,  but 
there  is  no  good  reason  why  they  should  not  occur,  particularly  after 
abrasion.  The  pulp  diseases  of  the  temporary  teeth  are  usually  of 
an  acutely  destructive  nature,  which  may  account  in  some  degree  for 
the  absence  of  reports  touching  this  subject. 


CHAPTER    XVII. 

DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

This  class  of  pulp  diseases  consist  of  those  of  an  acute  character, 
although  chronic  diseases  may  arise  as  sequelae  of  the  original  con- 
ditions. They  are  essentially  destructive  in  character  and  attended 
by  prompt  degeneration  of  the  pulp  tissues.  The  most  important 
clinically  are  those  having  an  evident  association  with  disorders  of 
the  bloodvessels  of  the  pulp. 

HYPER.ffiMIA  OF  THE  PULP. 

H^-pereemia  of  the  pulp  is  an  excess  of  blood  in  the  more  or  less 
dilated  vessels  of  that  organ.  It  is  of  two  forms:  active  or  arterial 
h}'per8emia,  and  venous  or  passive  h^^ersemia  or  congestion.  These 
two  classes  differ  in  their  probable  direct  causations  and  in  effects. 

Active  Hyperaemia  of  the  Pulp.  Definition.  Active  or  arterial 
hyperaemia  of  the  pulp  is  an  excess  of  blood  in  the  dilated  arteries 
and  capillaries  of  the  pulp. 

Causes.  The  most  common  cause  of  active  hj^ersemia  of  the  pulp 
is  a  lessening  of  the  non-conducting  covering  of  the  organ,  enamel,  and 
dentine,  leading  to  an  increased  response  and  continued  irritation  of 
the  pulp  through  thermal  stimuli.  A  similar  condition  consists  in  the 
presence  of  large  metallic  fillings  in  close  proximity  to  the  pulp,  through 
which  abnormal  thermal  stimuli  are  received.  Fillings  through  which 
prompt  pulp  response  to  thermal  changes  are  felt  are  a  direct  menace 
to  the  continued  health  of  the  pulp.  "The  vigorous  use  of  sandpaper 
disks  in  finishing  large  fillings  may  and  does  precipitate  an  attack  of 
pulp  hyperaemia."  The  loss  of  tooth  substance  mentioned  may  occur 
either  through  abrasion,  erosion,  fracture,  or  caries.  The  condition 
frequently  occurs  without  direct  exposure  of  the  dental  pulp,  and  at 
times  when  ca^dties  are  relatively  shallow.  Septic  dentine  beneath 
fillings  acts  as  a  cause  by  constantly  irritating  the  dentinal  fibrillse. 

Pulp  hyperaemia  may  also  be  caused  by  injury  to  the  apical  tissue 
of  a  tooth  containing  a  vital  pulp.  Acute  malocclusion  from  any 
cause,  a  blow,  or  overmalleting,   is   competent    to  produce  it.      An 


HYPEREMIA  OF  THE  PULP.  383 

abscess  upon  an  adjacent  tooth  may  have  its  area  of  hypersemia 
extend  into  the  apical  tissue  of  the  tooth  adjoining,  thus  producing 
hyperemia  of  the  pulp.  An  intense  hypersemia  or  inflammation  in 
the  pulp  of  one  tooth  may  by  reflex  action  produce  hyperaemia  with 
its  characteristic  response  to  hot  and  cold  applications  in  another  tooth. 
It  may  occur  from  the  presence  of  a  pulp  nodule.  An  aphthous  ulcer 
upon  the  gum  over  a  tooth  has  produced  arterial  hypersemia  of  the 
pulp  by  reflex  action. 

Apart  from  the  hypersemia  occurring  in  inflammation  and  that  due 
to  septic  dentine,  it  may  be  said  that  arterial  and  venous  hyperaemia 
are  mainly  due  to  non-septic  causes. 

Symptoms.  The  symptoms  of  arterial  hypersemia  vary  according  to 
the  degree  of  vascular  disturbance.  So  long  as  a  quick,  sharp  pain  is 
produced  by  contact  with  cold  or  hot  substances,  ceasing  immediately, 
and  only  reappearing  in  response  to  direct  stimuli,  no  serious  vascular 
disturbance  is  inferred;  but  when  paroxysms  of  sharp  pain  lasting  from 
many  minutes  to  hours  follow  upon  an  application  of  cold  to  a  carious 
cavity,  an  unbroken  enamel  surface,  a  filling,  or  an  area  of  erosion 
or  abrasion,  a  disturbance  of  the  vessels  of  the  pulp  is  indicated. 

The  pains,  in  the  absence  of  direct  irritation  are,  as  a  rule,  but 
vaguely  located.  During  parox}^sms  it  is  of  a  lancinating  character, 
and  usually  reflected  to  another  part  than  the  tooth  affected— e.  g.,  a 
sound  tooth  at  a  distance,  the  gum  between  or  above  the  teeth,  the 
ear,  the  eye,  the  supra-orbital  region,  the  infra-orbital  region,  the  scalp, 
the  chin,  the  arm,  etc. 

As  a  rule,  w^hen  an  upper  tooth  is  affected  the  pain  is  located  in 
the  superior  maxillary  division  of  the  fifth  nerve;  if  a  lower,  in  the 
inferior  maxillary  division.  The  pain  varies  in  intensity  from  a  vague 
uneasiness  to  an  acute  neuralgic  attack,  with  tender  spots  over  the 
emergence  of  the  nerve  tracks,  at  the  supra-orbital  and  infra-orbital  and 
mental  foramina.  The  neuralgic  pains  are  not  always  constant;  they 
may  disappear  from  the  second  or  third  division  of  the  fifth  nerve 
and  appear  in  the  first. 

The  proof  of  the  direct  connection  between  the  pulp  pain  and  the 
neuralgia  may  in  some  cases  be  clearly  made  out  by  the  thermal  test. 
When  a  jet  of  .cool  water  is  directed  against  the  tooth  whose  pulp  is 
affected,  it  may  produce,  in  addition  to  a  local  pain,  an  aggravation  of 
the  neuralgic  pains. 

Pathology  and  Morbid  Anatomy.  The  one  distinctive  and  character- 
istic anatomical  condition  associated  with  active  hyperaemia  is  an 


384 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


irregular  dilatation  of  the  vessels  of  the  pulp/  Fig.  359  represents 
a  section  of  the  pulp  of  a  tooth  extracted  during  a  paroxysm  of  acute 
pain — "acute  paroxysms  of  pain  lasting  for  an  hour  or  more  were 
occasionally  occurring  in  consequence  of  very  trivial  changes  of 
temperature;  the  condition  had  existed  for  several  weeks."  In  some 
cases  of  a  similar  character — i.  e.,  presenting  the  same  symptoms,  but 
extracted  during  an  interval  of  quiet — nothing  remarkable  is  pre- 


0 

Hyperaemia  of  the  dental  pulp,  showing  the  injection  of  the  vessels:  a,  a,  membrana  eboris,  or 
layer  of  odontoblasts;  b,  6,  &,  6,  vessels  distended  with  blood  ;  c,  c,  c,  c,  points  from  which  the 
blood  has  fallen  in  handling  the  section.     (Black.) 

sen  ted.  The  veins  of  the  bulb  may  be  abnormally  large  and  contain 
more  blood  than  usual,  while  the  arteries  will  be  almost  or  quite 
empty  and  the  injection  of  the  capillary  system  wanting;  that  is,  the 
affected  arteries  have  recovered  their  calibre,  if  not  their  tone.  Black 
found  the  varicose  enlargement  of  vessels  so  common  (Fig.  360)  as 
to  be  a  characteristic.  Salter^  first  called  attention  to  the  dilatation 
of  veins  into  ampullae,  describing  them  in  connection  with  ulceration 
of  the  pulp,  as  due  to  engorgement  and  overtension  of  the  veins. 


1  Black,  American  System  of  Dentistry. 
-  Dental  Pathology  and  Surgery. 


HYPEREMIA  OF  THE  PULP. 


385 


The  most  rational  explanation  of  the  dilatation  of  the  vessels  is  that 
it  is  an  irregular  paralysis  of  vessel  walls — i.  e.,  of  vasomotor  nerves. 
Whether  the  more  usual  painful  responses  of  the  pulp  to  thermal 
stimuli  are  due  to  the  stimulation  of  vasodilator  fibres,  which  causes 
hypersemia,  is  a  matter  of  doubt;  but  the  pathological  conditions 
noted  in  pronounced  hypersemia  signify  a  paralysis  of  vasoconstrictor 
fibres.  Subjected  to  repeated  overstimulation,  they  become  inactive 
and  the  vessel  walls  yield  to  the  pressure  of  the  blood  column.  Black's 
researches  indicate  that  the  vessel  walls  may  recover  their  tone  and  the 
vasoconstrictor  nerves  their  functional  activity  after  paralysis. 

Diagnosis  and  Prognosis.  Diagnosis  of  hypersemia  of  the  pulp  is 
made  through  observance  of  a  combination  of  signs  and  symptoms. 
The  symptoms  leading  to  its  detection  are  paroxysms  of  pain  induced 


Fig.  360. 


Dilated  bloodvessels  from  the  dental  pulp  in  hypersemia,  from  tooth  extracted  during  a 
paroxysm  of  intense  pain.      (Black.) 

by  thermal  stimuli,  and  a  history  of  pain  in  the  region  in  which  this 
response  is  elicited.  The  signs  of  the  condition  in  the  order  of  their 
importance  and  frequency  are  carious  cavities,  the  presence  of  large 
metallic  fillings,  deep  erosions  or  abrasions,  and,  again,  fractures 
exposing  the  dentine,  or  metallic  crowns  on  teeth  containing  vital 
pulps. 

It  is  to  be  remembered  that  arterial  hypersemia  may  be  of  several 
grades  of  severity,  according  to  the  vascular  disturbance. 

The  diagnosis  is  made  purely  by  differentiation.  The  causes  acting 
and  other  possible  pulp  diseases  must  be  fairly  considered  and  excluded 
before  a  certain  diagnosis  can  be  made.  As  a  rule,  the  absence  of 
pulp  exposure  and  the  character  of  the  response  to  thermal  tests  are 
the  decisive  phenomena. 

25 


386  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

The  temperature  of  the  water  used  in  testing  should  not  be  lower 
than  60°  F.,  and  should  be  applied  drop  by  drop.  A  normal  pulp  will 
rarely  respond  painfully  to  a  few  drops  of  water  at  the  temperature 
named,  flowed  into  a  cavity;  but  a  hypersemic  pulp  will  almost  invari- 
ably respond  vigorously.  As  a  rule,  a  current  of  air  from  a  chip 
blower  is  a  test  of  sufficient  severity. 

In  the  absence  of  a  carious  cavity  the  source  of  the  pain  is  to  be 
sought  in  large  fillings,  testing  each  tooth  by  dropping  cool  water  on 
the  filling;  in  cases  of  erosion  or  abrasion  the  test  is  made  upon  the 
exposed  dentine.  The  tooth  which  responds  with  a  quick  paroxysm 
of  intense  pain,  passing  away  slowly,  is  diagnosed  as  the  seat  of  pulp 
hypersemia. 

In  making  this  test  doubt  may  arise  as  to  which  of  two  adjoining 
teeth,  similarly  filled,  is  at  fault.  A  small  square  of  rubber-dam,  with 
a  single  hole  punched  in  its  centre,  may  be  passed  over  the  tooth  to 
be  tested,  thus  isolating  it. 

The  prognosis  of  arterial  hyperemia  is  favorable  for  pulp  conserva- 
tion in  cases  of  cavities  of  decay  which  admit  of  cleansing  without 
pulp  exposure,  and  in  which  the  paroxysms  have  not  been  too  severe 
or  too  often  repeated.  Properly  protected  from  thermal  shocks  the 
vessels  may  recover  their  tone.  It  is  also  favorable  in  cases  of  light 
blows  or  malocclusion  if  rest  of  the  apical  tissues  be  secured. 

It  would  be  favorable  in  cases  of  deep  erosions  which  can  be  filled 
with  non-conductors;  but  this  condition  is  rarely  seen  in  erosion.  It 
is  favorable  in  fractures  without  exposure  if  caps  can  be  secured  in 
place,  but  it  is  unfavorable  in  ordinary  abrasions  or  in  cases  of  sound 
teeth  largely  filled  with  gold,  or  in  sound  teeth  the  pulps  of  which  are 
irritated  without  evident  cause.  In  cases  of  actual  exposure  of  the 
pulp  it  contraindicates  attempts  at  conservation,  except  in  the  mildest 
varieties  and  most  favorable  circumstances,  and  then  only  when 
conservation  is  important. 

Treatment.  The  therapeutic  principles  involved  in  the  treatment 
of  this  condition  are,  the  removal  of  the  source  of  irritation  and  the 
securing  of  physiological  rest;  the  latter  can  only  be  secured  through 
the  removal  of  the  former.  The  treatment  is  directed  toward  imme- 
diate relief  of  the  existing  condition  and  the  prevention  of  its  recur- 
rence. If  a  carious  cavity  exist  it  is  to  be  freed  from  debris,  and  the 
grosser  portions  of  the  carious  dentine  are  removed;  the  pulp,  if 
unexposed,  is  to  have  the  layer  of  softened  dentine  covering  it  left 
unremoved. 


HYPEREMIA  OF  THE  PULP.  387 

Sedative  agents  are  imperatively  called  for;  of  those  used  the  most 
effective  being  the  oils  of  cloves  or  cinnamon,  equal  parts  of.  oil  of 
cloves  and  carbolic  acid,  equal  parts  of  carbolic  acid  and  camphor 
(phenol-camphor),  a  saturated  solution  of  thymol  in  alcohol  or  of 
menthol  in  chloroform,  or  a  combination  of  tincture  of  aconite  with 
cocaine.  These  agents  are  all  germicides  as  well  as  sedatives,  and, 
therefore,  sterilize  the  dentine  of  cavities  in  which  they  are  sealed. 

They  are  to  be  applied  upon  a  pledget  of  cotton  and  carefully 
secured  in  place  by  means  of  temporary  stopping,  soft  zinc  phosphate, 
or  facing  amalgam.  In  from  twenty-four  to  forty-eight  hours  the  tooth 
is  placed  under  the  rubber-dam  and  excavated ;  its  walls  are  varnished, 
and  over  the  wall  nearest  the  pulp  a  disk  of  softened  gutta-percha  is 
laid.  Over  this  zinc-phosphate  paste  is  flowed.  "Formagen"  or 
"  Jodo-Formagen  "  may  be  used  in  place  of  the  gutta-percha.  It  is 
usual  to  complete  such  fillings  with  zinc  phosphate  or  gutta-percha, 
to  remain  for  six  months  or  a  year.  The  conductivity  of  zinc  phosphate 
is  too  high  to  be  used  as  the  sole  material  over  pulps  which  have  been 
the  seat  of  pronounced  hyperaemia. 

If  the  pulp  be  exposed,  it  is  probably  the  part  of  wisdom  to  remove 
it  after  sedation  or  immediately  by  cocaine;  though  if  for  any  special 
reason  capping  be  demanded,  it  may  be  done. 

If  desired  the  protective  pocket-like  coverings  made  for  arsenical 
applications  may  be  utilized  for  the  reception  of  the  sedative  applica- 
tion.    (See  Coverings  for  Arsenic.) 

It  not  infrequently  happens  that  it  becomes  necessary  to  assist  the 
pulp  arteries  to  recover  their  tone  by  means  of  counterirritants  applied 
to  the  gum  over  the  apex  of  the  root.  This  is  especially  true  in  cases 
of  pulp  capping.  Dental  tincture  of  iodine  (a  saturated  solution  of 
iodine  in  alcohol)  is  to  be  applied  in  spots  to  the  gums,  or  a  mixture 
of  equal  parts  of  tincture  of  iodine  and  tincture  of  aconite  may  be 
painted  upon  the  gum.  A  mixture  made  of  two  parts  of  tincture  of 
aconite  and  one  part  of  chloroform  is  recommended  by  Jack,'^  to  be 
applied  to  the  cleansed  and  dried  mucous  membrane  by  means  of  a 
pad  of  cottonoid,  one-half  inch  wide  by  three-fourths  of  an  inch  long. 
It  should  be  held  in  place  by  the  finger  for  fifteen  seconds.  Tincture 
of  aconite  upon  cotton,  placed  in  the  rubber-cup  applicator  of  a  cata- 
phoric apparatus  and  held  against  the  gum  for  a  half-minute,  will 
produce  a  circumscribed  area  of  irritation  which  may  later  lose  its 
epidermis.     This  amount  of  irritation  is  valuable. 

1  American  Text-book  of  Operative  Dentistry. 


388  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

In  cases  of  abrasion  or  erosion  carbolic  acid'  is  applied ;  an  excava- 
tion having  a  retentive  form  is  made,  which  is  varnished  and  filled ;  or 
in  abrasion  the  pulp  may  require  removal.  A  tooth  containing  a  large 
metallic  filling  must  have  the  filling  removed,  and  after  reducing  the 
hypersemia  a  non-conducting  layer  must  be  placed  between  the  pulp 
and  the  filling.  The  precaution  should  always  be  taken,  when  the 
pulps  of  teeth  in  which  cavities  have  been  prepared  respond  unduly  to 
the  temperature  test,  to  cover  the  dentinal  walls  with  a  layer  of  non- 
conducting material.  In  the  absence  of  this  precaution  the  constant 
overstimulation  of  the  pulp  by  thermal  impulses  conducted  through 
the  metallic  filling,  may  at  any  time  result  in  hypersemia.  If  mild 
hyperfemia  occur  after  filling  with  metal  it  ordinarily  passes  away  after 
a  few  weeks.     The  fibrillae  at  first  rebel,  then  become  tolerant. 

In  the  cases  due  to  apical  irritation,  not  only  must  counterirritants 
be  applied  to  the  gum,  but  it  may  be  necessary  to  cap  one  or  two 
adjacent  teeth  in  order  to  guard  against  the  irritation  of  the  apical 
tissue  by  overocclusion.     (See  Non-septic  Apical  Pericementitis.) 

If  the  hyperaemia  is  of  a  gradual  onset  and  due  to  an  overoccluding 
filling  or  crown,  this  is,  of  course,  to  be  reduced. 

Idiopathic  hyperemia  occasionally  affects  teeth  in  which  there  is  no 
loss  of  enamel  or  dentine;  and  when  this  condition  occurs,  it  leads  to 
suspicion  that  the  pulp  is  the  seat  of  nodular  deposits;  though  cases 
have  occurred,  particularly  of  lower  incisors,  in  which  none  were 
found  after  devitalization.  Some  form  of  apical  traumatism  may 
also  be  looked  for.  Such  teeth  are  to  be  dried,  heavily  varnished,  and 
wedged  upon  both  sides  for  twenty-four  hours,  until  a  gutta-percha 
cap  can  be  fitted  to  them,  completely  enclosing  the  crown.  The  cap 
is  to  remain  and  to  be  renewed  until  the  tooth  responds  normally  to 
the  temperature  test. 

If  the  pulps  do  not  respond  to  this  treatment  they  are  to  be  devital- 
ized.    Counterirritants  may  also  be  used. 

Such  cases  may  be  very  obstinate  and  demand  relief  by  devital- 
ization of  the  pulp. 

The  test  of  success  of  remedial  measures  is  the  gradual  reduction 
of  response  to  slight  variations  in  temperature — /.  e.,  the  pulp  gradually 
bears  higher  and  lower  temperatures  until  approximately  a  normal 
tolerance  is  established. 

As  shown  by  Jack  this  varies  for  hot  applications  from  152°  F.  to 
118°  F.,  and  for  cold  ones  from  74°  F.  to  32°  F. 

In  order  to  determine  the  rate  of  tolerance  normal  to  the  individual, 


HYPEREMIA  OF  THE  PULP.  389 

he  suggests  that  sound  lower  incisors  be  isolated  by  the  rubber-dam 
and  tested  by  throwing  upon  them  first  water  at  a  temperature  of 
80°  F.  The  temperature  of  the  water  is  then  gradually  lowered  or 
raised  until  slight  pain  is  produced  by  the  test.  The  point  registered 
by  the  thermometer  will  be  the  normal  limit  of  thermal  tolerance  for 
the  particular  test. 

The  data  gained  are  useful  in  determining  the  progress  of  a  case 
of  hypersemia. 

A  lack  of  success  in  the  reduction  of  the  arterial  hypersemia  is 
evidence  that  the  more  severe  condition  of  venous  hypertemia  has 
supervened. 

In  the  devitalization  of  hypersemic  pulps  there  is  often  painful 
reaction  to  any  of  the  means  employed.  Sedatives  should  precede 
arsenical  applications,  and  if  at  any  time  arsenic  produce  a  painful 
hypersemia  or  aggravate  one  previously  existing,  it  must  be  removed 
and  sedatives  used  before  its  renewal,  or  it  may  be  applied  at  another 
portion  of  the  tooth  while  sedatives  are  kept  against  the  pulp. 

It  is  evident  that  such  a  grade  of  vascular  excitement  as  exists  in 
cases  of  exposed  dentine  is  quite  capable  of  producing  the  constructive 
diseases  of  the  pulp  described  as  secondary  dentine  and  pulp  nodules. 
On  the  other  hand,  inflammation  of  the  pulp  has  produced  resorption 
of  the  walls  of  the  pulp  chamber. 

Pulp  Irritation  from  Electric  Action.  It  is  of  quite  common 
occurrence  that  galvanic  electricity  causes  pulp  irritation.  The  cata- 
phoric current  too  long  continued  may  induce  a  hyperirritability  of 
the  pulp  amounting  in  some  cases  to  evidence  of  hypersemia,  which 
may  subside  under  proper  treatment  or  eventuate  in  pulp  death  from 
venous  hypersemia.  The  occasional  connection  of  a  newly  placed  or 
bright  amalgam  filling  with  a  gold  filling,  bridge,  plate  or  clasp,  through 
the  medium  of  saliva  or  food  (which  amounts  practically  to  the  same 
thing),  will,  at  times,  produce  painful  galvanic  shocks  in  a  vital  tooth. 
Dr.  Franz  Trauner^  has  reported  that  such  pain  has  been  felt  in 
devitalized  teeth.  This  is  outside  of  the  editor's  experience  and  should 
not  occur,  as  the  electric  current  is  a  test  for  pulp  vitality. 

Treatment.  With  cataphoresis,  the  mischief  being  accomplished, 
the  case  must  be  treated  as  other  arterial  hypersemias. 

In  the  case  of  shocks  from  the  presence  of  the  two  metals  it  may 
be  ignored  if  slight  and  the  filling  new,  as  it  will  probably  soon  pass 
away.      A  well-set  and  brightly  polished  filling  may  be  tarnished  if 

1  See  Dental  Cosmos,  1903. 


390  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

necessary  by  touching  it  with  a  1  per  cent,  sohition  of  silver  nitrate; 
or,  if  good  color  be  a  necessity,  the  pulp  of  the  tooth  may  be  well 
insulated  by  means  of  a  gutta-percha  substratum,  or  the  pulp  may  be 
devitalized.  If  the  fillings  be  in  adjoining  teeth  they  should  be  con- 
toured so  as  to  touch  if  possible.  If  in  the  same  tooth,  the  fillings 
should  be  connected  by  either  amalgam  or  gold. 

Painful  shock  is  sometimes  produced  by  the  animal  electricity 
discharged  from  the  operator  during  dry,  cold  weather.  It  usually 
occurs  when  the  finger  is  placed  upon  a  metal  filling  or  the  plugger 
point  is  returned  to  a  metal  filling.  Touching  the  metal  part  of  the 
chair  before  approaching  the  patient  will  obviate  this  disagreeable 
contact. 

Venous  Hyperaemia  of  the  Pulp.  Definition.  By  venous  hypersemia 
of  the  pulp  is  meant  a  condition  of  the  pulp  in  which  the  return  of  the 
blood  in  the  pulp  to  the  heart  is  mechanically  prevented. 

Causes,  Pathology,  and  Morbid  Anatomy.  But  two  causes  seem 
competent  to  produce  such  a  venous  hypersemia.  These  are:  (1)  a 
pre-existent  arterial  hypersemia;  (2)  thrombosis  of  vessels  at  the  apex 
of  the  pulp  canal. 

In  arterial  hypersemia  the  excess  of  blood  is  contained  in  enlarged 
capillaries  and  arterial  trunks.  The  enlarged  main  trunks  or  trunk 
at  the  apex  of  the  pulp  Tnust  compress  the  veins,  as  the  apex  of  the 
canal  is  unyielding.  In  proportion  to  the  severity  of  the  arterial 
hypersemia,  therefore,  are  the  emergent  veins  unable  to  remove  the 
blood  collected  in  the  capillaries  and  venules,  which  gradually  enlarge 
into  varicosities  in  consequence. 

Black  has  shown  that  the  diapedesis  of  red  corpuscles,  which  is  a 
characteristic  result  of  the  engorgement  of  the  veins  in  venous  hyper- 
semia (see  p.  81),  occurs  in  the  pulp.  Oedema,  which  usually 
accompanies  venous  hypersemia  in  other  situations,  cannot  well  occur 
in  the  pulp  because  of  its  unyielding  surroundings  (Fig.  361). 

It  is  possible,  however,  that  fluid  may  exude  into  the  perivascular 
spaces,  compressing  the  cellular  elements.  Black  has  shown  that 
deposits  of  lymph  may  thus  occur  in  pulpitis.  The  intense  congestion 
and  distention  of  the  vessel  walls  permit  a  free  diapedesis  of  red 
corpuscles  into  the  pulp  tissue.  These  go  through  the  stomata  of  the 
vessel  wall.  Disintegration  of  the  red  corpuscles  may  occur  and  the 
coloring  matter  of  the  corpuscles  may  be  diffused  through  the  dentine, 
giving  it  a  pink  discoloration  technically  known  as  suffusion.  The 
infiltrated  dentine  may  then  become  progressively  discolored  through 


HYPEREMIA  OF  THE  PULP. 


391 


the  characteristic  changes  of  color  noted  in  connection  with  gradually 
decomposing  haemoglobin — becoming  brown  or  blue,  and  finally  blue- 
black.  Cases  have  occurred  of  coronal  suffusion  in  which  the  pulp 
vitality  has  persisted.     The  vasomotor  paralysis  is  extreme. 

If  a  tooth  receive  a  blow  of  sufficient  severity,  its  pulp  may  die 
without  much  evidence  of  pulp  pain.  On  the  other  hand,  if  the  blow 
be  less  severe  it  may  give  evidence  of  an  arterial  hypersemia,  gradually 
increasing  in  severity. 

Fig.  361. 


i5^^*»f^#^^" 


Section  of  hyperaemic  pulp,  showing  aneurysmal  dilatation  of  the  vessels,  extravasations  of 
blood,  and  red  blood  disks  escaped  apparently  by  diapedesis:  a,  a,  dilated  vessels;  6,  6,  6,  ex- 
travasated  blood.  Besides  this,  red  blood  disks  are  plentifully  distributed  everywhere  in  the 
neighborhood  of  the  veins.     The  tooth  was  extracted  during  a  paroxysm  of  pain.     (Black.) 


In  the  former  case  it  is  probable  that  the  bruising  of  the  apical  tissue 
produces  a  condition  of  thrombosis  at  the  apex  which  involves  the 
pulp  by  shutting  off  both  its  afferent  and  efferent  vessels.  A  stagnation 
results,  and  death  from  lack  of  nutrition  occurs. 

In  the  latter  case  the  thrombosis  has  not  occurred,  but  an  arterial 
hyperemia  is  set  up  by  the  irritation  of  the  pulp  nerves  and  may  go 
on  to  venous  hyperaemia. 


392  DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 

It  is  quite  probable  that  tlie  death  of  the  pulp  in  pulpitis  is  due  to 
the  associated  venous  hypersemia. 

Kirk^  mentioned  an  interesting  case  of  venous  h}^eraemia  with 
intense  suffusion  of  all  the  teeth  as  the  result  of  hanging. 

Symptoms.  The  symptoms  of  this  condition,  in  the  absence  of 
definite  data,  can  only  be  inferential.  When  the  paroxysms  of  pain 
are  continuous,  instead  of  temporary — that  is,  when  the  pain,  instead 
of  temporarily  subsiding,  maintains  a  constant  intensity  for  hours,  and 
does  not  respond  promptly  to  sedative  therapeusis,  and  is  accompanied 
by  a  sense  of  fulness  rather  than  sharp  agony,  a  condition  of  serious 
venous  congestion  is  inferred.  The  case  from  which  Fig.  361  was 
taken  had  been  the  seat  of  intense  paroxysmal  pain  for  some  hours. 

Prognosis.  Perfect  recovery  from  this  condition  is  extremely 
doubtful,  so  that  if  the  pulp  be  not  intentionally  devitalized  and 
removed,  it  will  undergo  degenerative  changes.  The  fact  that  pulps 
have  remained  alive  for  years,  after  having  been  the  seat  of  marked 
congestion,  scarcely  warrants  the  attempt  to  save  so  seriously  crippled 
an  organ. 

Treatment.  The  prognosis  being  doubtful,  the  pulp  should  be 
obtunded  and  devitalized.  As  the  pulp  pain  does  not  ordinarily  yield 
to  sedatives  it  should  be  gently  exposed  if  the  excavation  does  not 
accomplish  its  exposure.  An  antiseptic  is  to  be  applied  and  by  means 
of  a  very  sharp  puncture  probe  the  pulp  is  to  be  delicately  punctured. 
A  free  flow  of  blood  follows,  which  relieves  the  vascular  engorgement. 
"When  this  is  accomplished  the  cavity  is  to  be  spinged  out  with  warm 
water  and  a  pellet  of  cotton  containing  a  saturated  solution  of  menthol 
in  chloroform  may  be  sealed  in  the  cavity,  or  simply  retained  by  means 
of  a  second  pellet  of  cotton  saturated  with  inspissated  tincture  of  ben- 
zoin or  chloro-percha.  After  twenty-four  hours  an  arsenical  application 
may  be  made  for  the  purpose  of  pulp  devitalization,  or  the  pulp  may 
be  removed  by  other  means  if  tolerated. 

The  extreme  paralysis  of  the  vessel  walls  is  occasionally  shown  by 
persistent  hemorrhage  after  depletion,  and  which  resists  all  effort  at 
limitation.  In  some  cases  the  intense  pain  may  continue  as  well. 
The  application  to  the  pulp  of  a  mixture  of  powdered  thymol  and 
dried  alum,  equal  parts,  taken  up  on  a  pellet  of  cotton  moistened  with 
a  saturated  solution  of  th\Tnol  in  alcohol,  has  proved  useful  in  some 
cases.  Adrenalin  chloride  solution  should  be  useful  in  this  connection. 
A  general  anodyne  may  be  required  for  relief  of  the  pain. 

1  Private  communication. 


INFLAMMATION  OF  THE  PULP.  393 

INFLAMMATION  OP  THE  PULP  (PULPITIS). 

Definition.  Pulpitis  is  the  occurrence  of  the  phenomena  of  inflam- 
mation within  the  pulp  tissue.  The  characteristic  diapedesis  of  leuko- 
cytes into  the  perivascular  tissues  must  have  occurred. 

Causes.  This  morbid  anatomy  is  usually  found  associated  with 
diseases  of  the  tooth  crown  or  pericemental  tissue  which  admit  bacteria 
to  the  pulp.  At  the  same  time  it  is  quite  possible  that  a  non-septic 
irritant,  such,  for  example,  as  a  partially  absorbed  extravasation  of 
red  corpuscles  or  undue  pressure  of  a  filling  upon  a  thin  lamina  of 
healthy  dentine  overlying  the  pulp,  or  an  escharotic  applied  to  the 
pulp  may  induce  the  characteristic  pathology  of  inflammation.  (See 
inflammation,  p.  83.) 

According  to  the  character  of  the  cause,  therefore,  inflammation  of 
the  pulp  may  be  divided  into  simple  and  infective.  It  may  be  that 
a  simple  inflammation  may  become  an  infective  one  owing  to  the 
association  of  bacteria — e.  g.,  the  pressure  of  a  foreign  body  may 
initiate  the  process  and  the  inflamed  pulp  become  a  soil  for  the 
propagation  of  the  bacteria  present. 

The  causes  of  pulpitis  may  be  grouped  under  three  headings: 

1 .  Mechanical  or  physical  causes,  which  irritate  by  acting  as  foreign 
bodies. 

2.  Chemical  causes,  which  act  as  irritants  by  either  producing  a  chemi- 
cal destruction  of  pulp  tissue  or  by  irritation  without  direct  destruction. 
In  the  former  case  the  dead  tissue  acts  as  a  foreign  body  against  which 
the  pulp  reacts  in  an  effort  to  cause  its  exfoliation  or  absorption. 

3.  Parasitic  or  infective,  which  cause  the  phenomena  of  infective 
inflammation. 

Pulpitis  is  classified,  according  to  its  extent,  into  partial  and  com- 
plete; according  to  its  duration,  into  acute  and  chronic;  according  to 
its  infective  character,  into  purulent  and  non-purulent;  and,  again, 
according  to  the  character  of  the  degeneration  which  follows  upon 
the  inflammatory  process.  While  pathologically  these  conditions  may 
be  clearly  differentiated  from  one  another,  they  may  be  reduced  to 
more  compact  groupings  according  to  their  clinical  significance.  For 
example,  acute  pulpitis  is  frequently  infective,  partial,  and  purulent; 
chronic  pulpitis  is  frequently  non-infective,  extensive,  non-purulent, 
and  indicative  of  secondary  degenerations. 

For  the  sake  of  convenience,  pulpitis  will  receive  a  clinical  di\dsion 
into  acute  and  chronic. 


394  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

Acute  Pulpitis.  By  acute  pulpitis  is  meant  that  form  of  inflam- 
mation of  the  pulp  which  runs  an  active  and  more  or  less  violent  course 
toward  pulp  death,  and  has  associated  with  it  acute  paroxysms  of 
pain. 

Causes.  The  causes  of  acute  pulpitis  are  direct  and  indirect, 
intrinsic  and  extrinsic;  the  vast  majority  of  cases  being  due  to 
extrinsic  causes.  The  direct  intrinsic  causes  are  hemorrhagic  ex- 
travasations accompanying  venous  congestion,  pulp  nodules,  and 
injury  of  the  vessels  at  the  apex  of  the  root.  The  direct  extrinsic 
causes  are,  perhaps,  invariably  associated  with  bacterial  invasion,  a 
possible  exception  being  the  pressure  of  filling  material  upon  a  thin 
elastic  lamina  of  softened  dentine,  covering  the  pulp.  The  dental 
pulp  is  intolerant  of  the  slightest  pressure,  and  rebels  vigorously  when 
subjected  to  compression.  Irritating  drugs  may  also  act  as  irritants — 
e.  g.,  zinc  chloride.  It  is  not  necessary^  that  the  pulp  should  be  exposed 
to  permit  bacterial  infection,  and  direct  or  extensive  bacterial  invasion 
is  probably  not  necessary  for  the  production  of  pulpitis.  The  waste 
products,  ptomains,  etc.,  of  bacteria,  may  find  their  way  to  the  surface 
of  the  pulp  via  the  dentinal  tubuli,  through  a  layer  of  softened  dentine, 
and  excite  inflammation.  It  is  extremely  probable  that  infection  of 
the  pulp  is  an  invariable  consecjuence  of  its  exposure;  but  as  a  pulp 
may  be  exposed  without  subjective  evidences  of  hypersemia  or  inflam- 
mation, it  follows  that  infection  does  not  necessarily  imply  inflam- 
mation, though  the  absence  of  acute  symptoms  may  be  accounted 
for  by  the  escape  of  the  effusions  into  the  cavity  of  decay.  The 
presence  of  a  gross  irritant,  such  as  a  mass  of  food  debris,  vegetable 
seeds,  bread-crumbs,  etc.,  in  contact  with  the  pulp  will  precipitate  an 
acute  inflammation  in  which  bacterial  relations  must  be  taken  into 
consideration. 

"The  severity  of  the  inflammation  does  not  appear  to  be  proportion- 
ate to  the  number  of  bacteria  present,  and  in  a  highly  inflamed  pulp  we 
may  be  able  to  find  but  few  bacteria.  .  .  .  The  conclusion  seems 
to  be  justified  that  the  inflammation  is  due  to  the  combined  action 
of  the  bacteria  and  their  products  (acids,  ptomains,  etc.)  with  which 
the  carious  dentine  becomes  impregnated."^  Goadby  has,  however, 
shown  that  the  streptococcus  brevis  and  bacillus  necrodentalis  may 
pass  through  the  tubules  of  even  secondary  dentine. 

Pulpitis  from  injury  of  the  vessels  at  the  apex  of  the  pulp  must  be 
mentioned.    It  may  occur  in  consequence  of  blows,  biting  upon  hard 

1  Miller,  Dental  Cosmos,  1894.  2  Ibid. 


INFLAMMATION  OF  THE  PULP. 


395 


substances,  too  rapid  wedging,  the  rapid  movement  of  teeth  in  ortho- 
dontia, and  the  progressive  loosening  of  teeth  in  pyorrhoea  alveolaris. 
In  these  cases  the  pericementum  is  also  affected  and  the  teeth  are  tender 
upon  percussion.  Pain  in  the  teeth  upon  assuming  the  recumbent  posi- 
tion; dull,  heavy  uneasiness  about  the  jaws,  and  inordinate  response 
to  thermal  stimuli,  particularly  to  heat,  point  to  pulpitis.  Bacteria 
from  an  abscess  on  an  adjoining  tooth  or  the  pressure  of  an  impacted 
tooth  may  also  act  as  causes. 

Morbid  Anatomy  and  Pathology.  In  determining  the  existence  of 
pulpitis,  no  matter  what  the  symptoms  which  have  presented  or  the 
condition  as  to  exposure,  etc.,  the  microscopic  examination  of  sections 
of  the  affected  organ  constitutes  the  only  decisive  test;  if  the  changes 
characteristic  of  inflammation  be  absent,  no  matter  what  the  symptoms, 


Fig.  362. 


Inflammation  of  dental  pulp:  a,  a,  normal  cells;  6,  6,  b,  6,  inflammatory  elements  ;  c,  cells  in 
process  of  division  (Vio  inch).     (Black.) 

pulpitis  did  not  exist.  The  essential  feature  of  the  process  is  emigration 
of  the  white  blood  corpuscles  from  the  small  veins  into  the  intercellular 
matrix  of  the  pulp.  At  first  the  inflammatory  elements  (leukocytes) 
are  scattered  through  the  spaces  between  the  pulp  cells  (Fig.  362); 
at  a  later  stage  the  territory  is  occupied  by  round  indifferent  cells  alone. 
The  inflammation  may  be  widespread,  as  shown  in  Fig.  363,  or  may 
be  localized  to  some  portion  of  the  pulp,  as  one  horn  of  a  pulp;  Black 
noted  also  inflammatory  action  occurring  in  small  islands  (Fig.  364). 
Swelling  of  the  pulp — exudation — cannot  occur  unless  there  be  a 
break  in  the  wall  of  the  pulp-chamber  through  which  additional  space 
can  be  gained.  Black  has  recorded  that  "he  found  beneath  the  layer 
of  odontoblasts  in  the  region  of  an  exposure  an  unmistakable  deposit 


396 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


of  inflammatory  lymph.  The  case  had  a  history  of  severe  toothache 
for  two  clays,  two  weeks  previously.  The  pulp  exhibited  evidences  of 
previous  extravasations  of  blood  from  hypersemia." 


Fig.  363. 


Section  of  dental  pulp,  showing  the  invasion  of  the  inflammatory  process  along  the  course  of 
the  veins — the  diapedesis  of  the  white  blood  corpuscles. 

There  is  evidence  that  the  pulp  may  recover  from  attacks  of  inflam- 
mation, and  that  resolution  occurs.  In  some  cases,  as  shown  under  the 
head  of  calcareous  degeneration,  the  tissues  may  become  infiltrated 


llinute  inflammatory  focus  within  the  tissues  of  the  pulp:  a,  a,  arterial  twigs;  6,  a  nerve  bundle; 
C,  collection  of  leukocytes.      (Black.) 

with   calcic   material.      In    others,    chronic   degenerative   changes — 
inflammatory  degeneration — may  supervene. 

The  cases  thus  far  described  have  been  given  as  non-infective, 
simply  because  their  infective  character  has  not  been  clearly  made  out, 
although  it  is  very  probable  that  they  are  infective. 


INFLAMMATION  OF  THE  PULP.  397 

Suppuration  of  the  pulp  is  a  common  accompaniment  of  pulp 
inflammation;  this  being  necessarily  infective,  will  be  described 
separately. 

GaskelP  has  reported  a  case  where  a  central  incisor  entirely  free 
from  caries  exhibited  on  its  palatal  aspect  a  pinkish  tinge,  which 
increased  in  depth  until  the  enamel  overlying  crushed  in,  revealing 
the  pulp  of  the  tooth  lying  immediately  beneath;  there  had  been  a 
resorption  of  a  large  mass  of  the  dentine  lying  between  the  pulp  and 
the  enamel.  The  pulp  was  removed  and  the  tooth  filled.  No  history 
is  given  as  to  the  condition  of  the  root,  whether  resorption  had  occurred 
there  or  not.  Shortly  after,  the  adjoining  central  incisor  exhibited 
a  like  pink  coloration,  which  increased,  leading  to  the  inference  that 
resorption  was  in  progress  in  this  tooth  also.  At  the  suggestion  of 
E.  C.  Kirk  the  patient  received  continued  doses  of  arsenic  iodide  and 
the  compound  syrup  of  the  hypophosphites,  in  the  hope  of  inducing 
a  general  and  local  constructive  metamorphosis.  This  treatment  was 
followed  by  a  gradual  disappearance  of  the  pink  coloration,  an  evidence 
of  a  redeposition  of  dentine.  In  the  absence  of  histological  data  it  is 
impossible  to  state  just  what  was  the  nature  of  the  repair  tissue  in 
this  particular  case,  but  Miller^  has  shown  that  the  pulp  may  take  up 
a  resorptive  function  and  remove  dentine  which  may  later  be  deposited 
as  anomalous  tissue.  The  new  dentine  does  not  contain  tubules,  but 
has  the  characteristics  of  cemental  tissue^  (osteodentine),  or  even  bone 
with  Haversian  systems*  (Fig.  365).  This  process  has  its  analogue 
in  the  tusks  of  elephants  and  also  in  the  production  of  Howship's 
lacunae  in  the  resorption  of  the  cementum  by  the  pericementum,  these 
lacunae  later  being  filled  up  with  cementum. 

Symptoms.  The  early  stage  of  inflammation  is  an  arterial  hyper- 
semia,  and  as  the  leukocytes  collect  in  the  venules  a  venous  hypersemia 
is  established.  No  matter  how  far  the  area  of  stasis  extend,  beyond 
it  will  exist  an  area  of  arterial  hypersemia.  Owing  to  the  enclosing 
canal  walls  and  constricted  apex  a  general  venous  hypersemia  may  be 
established  which  causes  the  death  of  the  pulp. 

In  view  of  these  facts  it  is  not  surprising  that  the  symptoms  of  pulp 
inflammation  take  on  somewhat  the  characteristics  of  both  arterial 
and  venous  hypersemia.    The  diapedesis  of  leukocytes  and  exudation 

1  Proceedings  of  the  Academy  of  Stomatology,  Philadelphia,  1S95. 
-  D.ental  Cosmos,  August,  1901. 

3  Hopewell-Smith,  Histology  and  Patho-histology  of  the  Teeth. 
*  Salter,  Dental  Surgery  and  Pathology^ 


398  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

of  fluid  cause  the  phenomena  of  heavy  boring  pain  and  a  feehng  of 
internal  pressure. 

The  pulp  may  be  exposed  and  no  symptoms  be  present.  A  sudden 
pressure  of  food  or  toothpick,  suction  upon  the  pulp  or  the  contact  of 
cold  or  hot,  salt,  sweet,  or  acid  substances  may  excite  an  attack  of 
throbbing  or  lancinating  pain.  This  may  be  localized  in  the  tooth  or 
may  be  reflected  to  other  teeth  or  the  parts  mentioned  under  hypersemia. 

The  assumption  of  the  recumbent  position  permits  an  increased 
flow  of  blood  into  the  paretic  vessels  of  the  pulp  and  increased  suffer- 
ing results  in  correspondence  with  the  law  that  inflamed  parts  are 

Fig.  365. 


Resorption  of  the  walls  of  the  pulp  chamber  and  redeposition  of  new  calcific  matter  :  a.  pulp 
chamber;  6,  c,  d,  portions  of  resorption  areas  not  refilled  and  waUed  off  by  the  new  deposit- 
forming  cavities  occupied  originally  by  the  pulp  tissue.      (Miller.) 

always  more  painful  in  the  dependent  position.  (See  Pathological  First 
Dentition.)  Indeed,  recumbency  is  sufiicient  at  times  to  induce  a 
paroxj^sm  in  a  comparatively  quiet  but  inflamed  pulp.  Under  a 
capping  or  filling  pressing  on  the  pulp  or  thin  dentine  the  pain  may 
begin  as  a  slight  pain  and  gradually  increase  in  intensity,  or  it  may 
respond  as  a  sudden  agony,  beginning  even  some  time  after  the  oper- 
ation. In  the  later  stage  of  pulp  inflammation  the  pain  is  of  a  heavy, 
boring,  continuous  character,  the  pericementum  becomes  somewhat 
hypersemic,  and  the  tooth  responds  to  tapping.  In  case  of  a  highly 
irritable  pulp,  however,  the  concussion  of  the  pulp  produced  by 
tapping  may  readily  cause  pain. 


IXFLAMMATIOX  OF  THE  PULP.  399 

In  pulpitis  the  pulp  responds  both  to  heat  and  cold,  but,  as  a  rule, 
more  to  the  former  than  to  the  latter. 

Diagnosis.  The  diagnosis  is  largely  inferential  and  made  by  obser- 
vation of  the  symptoms  and  conditions  existing.  The  pulp  may  be 
exposed  or  closely  approached  by  caries,  or  the  pulp  may  be  approx- 
imated by  a  large  filling.  If  there  be  a  leak  about  the  filling  a  septic 
fluid  or  actual  decay  beneath  the  filling  may  be  the  exciting  cause. 
In  the  absence  of  evident  causes  such  sepsis  is  always  to  have  con- 
sideration, and,  if  necessary,  the  filling  must  be  removed  and  tests 
applied.  The  more  obscure  causes,  such  as  abscesses  upon  adjoining 
teeth,  infection  from  the  pericemental  tract  in  the  course  of  pyorrhoea, 
looseness  of  teeth  or  traumatisms,  are  to  be  carefully  considered.  If 
the  tooth  involved  be  uncertain,  each  tooth  should  be  placed  under 
rubber-dam  and  tested  thoroughly. 

Prognosis.  The  prognosis  is  always  bad  for  the  comfortable  conser- 
vation of  the  pulp,  and  it  should  be  removed  and  the  canal  filled. 

Treatment.  The  treatment  of  pulpitis  involves  the  reduction  of  the 
amount  of  blood  in  the  vessels  of  the  pulp,  the  sterilization  of  the 
infected  area,  and  the  relief  from  the  pain.  It  is  usual  to  excavate  the 
cavity  of  decay  thoroughly  enough  to  remove  from  over  the  pulp 
decayed  dentine  which  would  prevent  the  action  of  remedies,  or  act 
as  irritants  per  se.  The  cavity  is  then  washed  and  one  of  the  essential 
oils  or  phenol-camphor,  saturated  solutions  of  cocaine  in  glycerin, 
thymol  in  alcohol,  or  menthol  in  chloroform,  or  a  mixture  of  acetate 
of  morphine  with  oil  of  cloves  or  creosote  is  placed  in  it  on  cotton. 
During  the  half-hour  succeeding  the  application  the  pulp  should  give 
some  indication  of  relief.  If  it  be  somewhat  decided,  a  portion  of  the 
remedy  used  should,  if  possible,  be  sealed  in  the  cavity  for  twenty- 
four  hours.  The  covering  may  be  prepared  first  as  for  arsenic.  (See 
Coverings  for  Arsenic.)  If  not  possible  to  seal  it  in,  it  may  be  covered 
with  cotton  saturated  with  a  varnish  made  by  evaporating  tincture  of 
benzoin.  This  varnish  hardens  like  sandarac  varnish,  but,  unlike  it, 
is  not  irritant. 

If  after  the  first  half-hour  no  indication  of  relief  has  been  obtained, 
it  is  well  to  expose  the  pulp  and  to  relieve  the  engorged  vessels  by 
delicately  puncturing  it.  (See  Extirpation  of  Pulp.)  After  exposing 
the  pulp  it  will  perhaps  exude  a  bead  of  pus,  which  makes  the  diag- 
nosis one  of  pulp  suppuration.  After  free  bleeding,  which  may  be 
encouraged  by  means  of  warm  water,  the  sedatives  will  usually  act. 
It  may  be  necessary  at  times  to  employ  general  anaesthesia  (nitrous 


400  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

oxide  gas)  as  a  means  to  obtain  free  bloodletting.  Everything  being 
prepared,  the  patient  is  anaesthetized  and  the  bulb  of  the  pulp  cut 
out,  or  in  a  single-rooted  tooth  the  entire  pulp  may  be  taken  out. 

At  times  cocaine  pressure  anaesthesia  is  effective  at  least  for  the 
removal  of  the  bulb  of  the  inflamed  pulp,  and  sometimes  of  the 
entire  pulp. 

In  case  of  partial  extirpation,  not  only  is  free  bleeding  induced,  but 
the  diseased  pulp  tissue  is  largely  removed.  When  hemorrhage  ceases 
arsenic  may  be  applied.  If  the  hemorrhage  be  obstinate  the  application 
of  powdered  thymol  and  dried  alum  may  be  used.  (See  Venous  Hyper- 
semia.)  ^Yhen  sedatives  are  used  upon  the  pulp,  counterirritants 
applied  to  the  gum  are  aids  of  great  value  and  are  to  be  used  as 
described  under  arterial  hypersemia.     (See  p.  387.) 

Instead  of  these  the  principle  of  depletion  may  be  employed.  Deep 
cuts  may  be  made  with  a  sharp  bistoury  in  the  gum  overlying  the 
root  apex.  The  anastomosis  with  the  vessels  of  the  apical  tissue  is 
expected  to  cause  the  cuts  to  act  as  openings  made  in  veins  leading 
from  the  inflamed  pulp.  According  to  Nancrede,  depletion  on  the 
venous  side  of  an  inflamed  area  markedly  reduces  engorgement.  In 
addition  to  these  measures  catharsis  is  a  valuable  means  of  derivation ; 
a  tablespoonful  of  sulphate  of  magnesia  is  to  be  dissolved  in  a  goblet 
of  water  and  taken  internally. 

If  the  pain  be  obdurate  and  its  return  feared,  two  one-eighth-grain 
sulphate  of  morphine  tablets  may  be  dispensed,  preferably  by  the 
operator,  to  be  taken  only  in  case  of  severe  pain  and  an  hour  apart. 
Acetanilid  and  phenacetin  are  also  useful. 

The  following  is  a  useful  anodyne  and  antineuralgic  prescription: 

9- — Phenacetin , 

Acetanilid,  da    gr.  xxx. 

Quinia  sulph. ,  gr.  xv. — M. 

Divide  into  six  capsules. 
Sig:  One  morning  and  evening. 

Quiet  of  the  pulp  must  be  secured  before  an  arsenical  application 
is  made  or  the  latter  merely  increases  the  irritation  instead  of  promptly 
devitalizing.  Should  such  an  irritation  occur  or  be  feared  arsenic  may 
be  sealed  in  an  opening  made  in  another  part  of  the  tooth  (a  "pocket")^ 
with  a  view  to  devitalizing  the  pulp  through  an  avenue  of  healthy  pulp 
tissue.  At  the  same  time  the  pulp  may  be  quieted  by  applications 
made  in  the  cavity  of  decay. 

Instead  of  drilling  a  special  pit  the  arsenic  may  be  applied  at  a 

1   Flagg. 


SUPPURATION  OF  THE  PULP. 


401 


portion  of  healthy  dentine  in  the  cavity  which  is  at  some  distance  from 
the  orifice  of  exposure;  over  the  latter  the  analgesic  may  be  placed. 


SUPPURATION  OF  THE  PULP. 


Fig.  366 . 


Definition.  By  suppuration  of  the  dental  pulp  is  meant  a  formation 
of  pus  on  its  surface  (ulceration)  or  in  its  substance  (abscess).  It 
occurs  both  as  an  acute  and  as  a  chronic  affection. 

Causes.  The  immediate  cause  of  suppuration  of  the  pulp  is  the 
ingress  of  pyogenic  organisms  to  the  pulp.  As  in  inflammation  of  the 
pulp,  while  usually  associated  with  direct  exposure  of  the  pulp,  suppu- 
ration may  occur  in  pulps  covered  by 
softened  or  even  unsoftened  dentine. 

Arkovy^  (Fig.  366)  first  observed  in- 
fection of  the  pulp  while  still  covered 
by  a  layer  of  unsoftened  dentine. 

Goadby  has  shown  that  micro-organ- 
isms may  penetrate  even  secondary  den- 
tine, a  condition  not  infrequently  seen. 

Miller  states  that  sections  of  the 
overlying  dentine  in  a  case  of  suppura- 
tion of  the  pulp  showed  the  same  forms 
of  bacteria  as  were  found  in  the  pulp  itself. 

Bacteria  which  have  entered  the  body 
through  wounds,  etc.,  may  be  deposited  in  the  pulp  as  well  as  in 
any  other  part  of  the  body,  wherever  there  may  be  a  locus  minoris 
resistentice  at  the  time. 

While  bacteria  may  thus  enter  from  the  circulation,  there  is  usually 
abundant  opportunity  for  their  entrance  from  the  mouth. 

Suppuration  of  the  pulp  is  a  not  infrequent  sequel  of  the  capping 
of  pulps  which  have  given  evidence  of  a  previous  hypersemia  or  inflam- 
mation. 

Morbid  Anatomy  and  Pathology.  Anatomically  pulp  suppuration, 
purulent  or  pyogenic  pulpitis,  is  of  two  general  varieties;  one  begins 
upon  or  close  to  the  surface  of  an  exposed  pulp,  and  gradually  destroys 
the  organ  through  a  process  of  progressive  ulceration  (Fig.  367); 
the  second,  that  confined  in  the  substance  of  the  pulp,  causes  the 
gradual  destruction  of  a  part  or  all  of  the  pulp  through  the  formation 
of  circumscribed  abscesses  (Fig.  368). 


Invasion  of  pulp  by  micrococci. 

(Arkovy.) 


Diagnostik  der  Zahnkrankheiten. 
26 


402 


DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 


Ulceration  of  the  Pulp.  Of  these  two  forms,  ulceration  is  the  more 
common.  The  capillaries  (Fig.  367)  are  blocked  with  coagulated 
blood  (they  are  left  open  in  the  illustration  to  clearly  mark  their 
position);  the  intercapillary  meshwork  is  occupied  by  inflammatory 
exudation;  the  surface  of  the  pulp  is  eroded,  and  covered  with  pus- 
corpuscles;  the  ulcerative  process  is  undermining  the  layer  of  odonto- 
blasts. The  suppurative  process  penetrates  the  body  of  the  pulp, 
following  the  direction  of  its  veins  and  hollowing  out  the  organ  into 

Fig.  367. 


A,  diagram  of  lower  molar  viith  caries  at  a  which  exposes  the  pulp;  the  darkened  portion  at  6 
shows  the  extent  of  the  inflammation;  the  rest  of  the  organ  was  free  from  inflammatory  change. 
B,  illustration  of  the  inflamed  tissue,  showing  a  part  destroj'ed  by  suppuration  at  a;  the  odon- 
toblasts are  undermined  at  fc ;  the  bloodvessels  which  were  filled  with  blood  clot  in  the  section 
are  left  blank  here,  that  they  may  be  more  apparent.     (Black.) 


a  deep  cavern.  Black  regards  the  persistence  of  the  layer  of  odonto- 
blasts as  indicating  an  inferior  vitality,  as  it  shows  they  are  less  suscept- 
ible of  change  of  form  than  the  other  cells  of  the  organ. 

The  process  of  ulceration  may  continue  for  weeks  or  months  until 
the  entire  organ  has  been  destroyed  molecularly.  The  necrotic  portions 
undergo  putrefactive  decomposition,  probably  passing  through  the 
same  stages  that  any  albuminous  substance  passes  in  its  serial  decom- 
position, into  the  end  products — ammonia,  carbon  dioxide,  hydrogen 
sulphide,  and  water. 


SUPPURATION  OF  THE  PULP. 


403 


"Very  interesting  and  instructive  results  were  obtained  by  examining 
material  from  different  parts  of  the  same  tooth.  In  the  case  illustrated 
in  Fig.  369  the  pulp  chamber  at  a  was  wide  open  and  filled  with 


Fig.  368. 


Acute  suppurative  pxilpitis  in  the  coronal  portion:  J,  intensely  inflamed  horn;  ^.abscess;  V, 
bloodvessels  engorged  -with  blood;  S,  superficially  inflamed  horn;  N,  [nest  of  inflammation. 
X  10.     (Bodecker.) 

food  particles,  which  had  a  foul,  half-putrid  odor;  at  b  the  pulp  was 
putrid  and  foul-smelling;  at  c  there  was  a  small  abscess,  filled  with 
pure  white  pus,  while  the  tissue  between  this  point  and  the  apex  of  the 
root  was  highly  inflamed  and  bright  red.      Material  from  the  pulp 


404 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


chamber  (Fig.  369,  a)  contained  the  forms  shown  in  Fig.  370;  material 
from  point  b  those  shown  in  Fig.  371,  and  from  the  point  c  those  shown 
in  Fig.  372.  We  perceive  a  gradual  diminution  of  the  large  cocci,  and 
the  appearance  of  small,  delicate  cocci  and  diplococci"  (Miller).^ 

Symptoms.  If  the  cavity  of  decay  be  open  the  pus  and  serous 
exudate  may  freely  escape,  so  that  the  symptoms  may  not  exceed  a 
dull,  gnawing  pain  which  is  usually  reflex  in  character. 

As  a  rule  the  response  to  cold  will  be  much  delayed  or  even  absent. 
Intense  pain  may  exist  when  the  pus  cannot  find  exit  owing  to  food 
debris  being  massed  in  the  pulp  chamber,  or  owing  to  the  presence 


Fig.  369. 


Fig.  370. 


Fig.  371. 


Fig.  372. 


Micro-organisms  found  in  cultures  from  gangrenous  pulp.    (Miller.) 

of  a  filling  or  mass  of  secondary  dentine.  The  case  then  resembles, 
and  practically  becomes,  one  of  abscess  of  the  pulp. 

The  chief  diagnostic  feature  of  pulp  ulceration  is  the  presence  of 
the  subacute  inflammatory  symptoms  described  above  and  the  pres- 
ence of  a  pulp  partially  removed  by  decomposition  of  its  upper  portion. 

Thus,  if  the  pulp  chamber  be  open  at  one  horn,  and  a  probe  may 
be  passed  into  it  for  a  short  distance  until  it  comes  into  contact  with 
an  irritable  portion  of  pulp  and  when  withdrawn  have  the  odor  of 
putrefaction,  the  diagnosis  is  clear— loss  of  pulp  substance  by  putre- 
factive changes,  presumably  by  suppuration.  Many  phases  of  this 
condition  may  be  seen;  thus  in  an  extreme  case  one  canal  of  a  lower 


1  Dental  Cosmos,  1894. 


SUPPURATION  OF  THE  PULP.  405 

molar  contained  a  highly  irritable  vital  filament  of  pulp  extending 
but  one-quarter  inch  from  the  apical  foramen;  a  second  canal  was 
entirely  occupied  by  a  perfectly  vital  but  ulcerating  filament;  the 
third  canal  contained  an  entirely  dead  pulp.  The  bulb  of  the  pulp 
had  disappeared,  doubtless  by  suppuration. 

Treatment.  The  treatment  of  pulp  ulceration  in  its  early  stages 
involves  the  opening  of  the  orifice  of  exposure,  the  sterilization  of 
the  superficies  of  the  pulp,  and  pulp  removal. 

Superficial  sterilization  may  be  accomplished  by  removing  the  pus 
or  putrefactive  material  present  by  means  of  warm  3  per  cent,  hydrogen 
dioxide  or  a  50  per  cent,  solution  of  meditrina.  The  saturated  solutions 
of  thymol  in  alcohol  or  menthol  in  chloroform,  or  2  per  cent,  formal- 
dehyde 'may  be  sealed  in  position  against  the  pulp  for  twenty-four 
hours  as  a  sedative  antiseptic.  The  application  of  arsenic  may  then 
be  safely  made. 

In  favorable  cases  the  bulb  of  the  pulp,  or  even  the  entire  pulp, 
may  be  removed  at  the  first  or  second  sitting  by  means  of  cautiously 
applied  cocaine  pressure  anaesthesia.  In  some  cases,  however,  the 
patient  will  rebel. 

When  a  part  of  the  canal  filaments  alone  remain,  after  syringing 
to  remove  pus,  the  pressure  anaesthesia  may  be  resorted  to.  A  long 
thread  of  spunk  is  cut  from  the  sheet,  saturated  with  carbolic  acid 
or  carbolic  acid  and  cocaine,  and  gently  packed  into  the  canal  against 
the  pulp  filament.  Pressure  with  vulcanizable  rubber  is  now  pro- 
duced and  after  a  few  minutes  the  pulp  will  be  sterilized  and  anaesthe- 
tized sufficiently  for  removal.  Puncturing  is  also  useful  at  times  (which 
see).  Arsenic  may  be  cautiously  placed  on  cotton  half-way  up  a  canal 
against  such  a  pulp  filament.  Another  method  consists  of  packing 
a  thread  of  cotton  dipped  in  carbolic  acid  tightly  against  the  filament, 
in  which  thrombosis  is  thus  induced. 

Abscess  of  the  Pulp.  Abscess  of  the  pulp  is  usually  situated  near 
the  point  of  exposure  of  the  organ.  It  may  be  confined  to  one  horn 
of  the  pulp,  or  may  involve  nearly  the  entire  substance  of  the  pulp, 
the  peripheral  tissue  of  the  pulp  being  unbroken.  Abscess  may  exist 
at  some  distance  beneath  the  surface  of  the  pulp,  and  the  latter  be 
still  covered  with  a  layer  of  dentine.  Burchard  once  uncovered  the 
horn  of  a  molar  pulp  which  was  covered  by  a  lamina  of  hard  dentine, 
and  no  fluid  appeared;  but  upon  passing  a  sharp  probe  into  the  white 
area  of  exposure  for  over  one-eighth  of  an  inch  or  more  there  was  a 
free  flow  of  pus  which  quickly  filled  the  larger  carious  cavity.    A  pulp 


406 


DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 


removed  entire  from  a  tooth  and  wliich  was  yellowish-white  in  color 
and  unbroken  showed  upon  section  its  interior  hollowed  out  into  an 
enormous  abscess  cavity  (Fig.  374).  The  bloodvessels  were  blocked; 
the  peripheral  tissues  were  unaltered ;  between  the  odontoblasts  and  the 
abscess  cavity,  the  latter  lined  with  pus  corpuscles,  evidences  of  inflam- 
mation were  plenty.  Black  found  that  the  odontoblasts  retained  their 
form  after  neighboring  cells  of  the  pulp  had  been  destroyed. 

Miller's^  researches  show  a  preponderance  of  cocci  and  micrococci 
in  cases  of  enclosed  abscess;  cocci  and  diplococci  were  of  constant 
occurrence.    Many  of  the  forms,  both  cocci  and  bacilli,  were  cultivable 

Fig.  374. 


Transverse  section  of  inferior  bicuspid  pulp,  one-half  diagrammatic:  a,  abscess  ca\'ity;  b,  em- 
bryonic cells  at  the  periphery  of  the  abscess  cavity  ;  c,  occluded  bloodvessels.    (Burchard.) 

upon  gelatin  and  agar-agar.  Some  of  them,  cocci  and  bacilli,  brought 
about  the  liquefaction  of  gelatin;  others  did  not.  So  that  it  must  be 
inferred  that  infective  inflammation  and  necrosis  of  the  pulp  may 
occur  without  suppuration.  (See  Gangrene  of  the  Pulp.)  In  some 
instances  streptococci  were  found.  In  the  freely  exposed  pulps 
varieties  of  organisms  were  found  which  would  render  clear  the 
possibility  of  a  general  infection  by  way  of  the  dental  pulp. 

Symptoms.  The  usual  symptoms  are  as  follows:  In  a  tooth  con- 
taining an  enormous  filling,  one  in  which  the  pulp  has  been  exposed, 
or  in  a  tooth  ha\nng  a  large  carious  cavity,  the  patient  gives  a  history 
of  discomfort  or  decided   pain,   appearing   at  intervals,   sometimes 


1  Dental  Cosmos,  1894. 


SUPPURATION  OF  THE  PULP.  407 

appearing  and  disappearing  suddenly,  the  existing  condition  having 
been  ushered  in  by  dull,  gnawing  pain,  which  is  usually  not  positively 
located,  although  it  may  be.  The  pain  grows  in  intensity,  and,  in 
contradistinction  to  the  pulp  conditions  previously  described,  pain  is 
relieved  instead  of  increased  by  applications  of  cold.  It  may  be, 
however,  that  the  prolonged  contact  of  ice-water  may  induce  a  response. 
The  response  to  heat  is  marked,  so  that  a  mouthful  of  hot  coffee  or 
even  the  warmth  of  the  tongue  may  precipitate  an  attack  of  severe 
and  continued  pain.  Pain  produced  upon  passing  from  a  warm  to 
a  cold  atmosphere,  and  vice  versa,  is  also  symptomatic.  If  the  pulp 
be  freely  exposed  and  pricked  with  a  sharp  instrument,  a  flow  of  pus 
follows  in  many  cases,  and  the  relief  is  almost  immediate.  In  the 
earlier  stages  a  period  of  throbbing  pain  may  follow  evacuation  of 
the  pus. 

In  other  cases  the  response  to  heat  may  decrease  until  it  is  almost 
absent,  and  the  case  only  be  seen  when  evidences  of  the  action  of 
bacterial  products  upon  the  pericementum  appear,  which  they  usually 
do  in  the  later  stages  of  pulp  suppuration,  when  the  tooth  becomes 
loose,  extruded,  and  tender  upon  percussion. 

The  symptoms  of  pericemental  disturbance  may  simulate  those  of 
incipient,  acute,  apical  abscess,  even  though  a  quarter  of  an  inch  or 
more  of  apical  pulp  tissue  exist  in  a  vital  though  highly  inflamed 
condition.  Upon  clinical  evidence  it  is  assumed  that  the  inflammation 
of  the  pulp  produces  inflammation  of  the  apical  tissue  (Fig.  375). 
In  one  case  the  gum  and  contiguous  parts  about  an  upper  molar 
were  swollen,  apical  abscess  diagnosed,  and  a  free  flow  of  pus  fol^ 
lowed  by  blood  obtained  upon  opening  the  crown.  An  examination 
made  twenty-four  hours  later,  after  symptoms  had  subsided,  demon- 
strated all  three  pulp  filaments  to  be  alive  when  a  'post  hoc  diagnosis 
of  extensive  abscess  of  the  pulp  was  made.  If  untreated,  symptoms  of 
pulp  and  pericemental  disturbance  may  disappear  for  weeks  or  months ; 
but  if  the  parts  be  not  perfectly  sterilized  and  reinfection  prevented, 
it  is  only  a  question  of  time  when  septic  pericementitis  will  arise. 

Diagnosis.  The  most  valuable  diagnostic  sign  is  the  peculiar 
reaction  to  thermal  stimuli — the  decreasing,  then  absent  response  to 
cold,  and  the  increasing  reaction  to  applications  of  heat.  This  reaction, 
together  with  the  continued  gnawing  and  full  sensation  in  the  tooth, 
usually  affords  a  diagnosis  which  is  confirmed  by  evacuating  pus 
from  the  pulp,  which  exudes  usually  as  a  minute  bead  followed  by 
blood,  though  the  reverse  order  may  obtain. 


408  DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

In  cases  where  several  teeth  are  involved  in  the  diagnosis,  differ- 
entiation is  made  by  isolation  of  each  tooth  by  means  of  a  small  square 
of  rubber-dam.  The  thermal  test  is' then  applied.  The  presence  of 
a  quantity  of  secondary  dentine  will  confuse  by  causing  dulness  of 
response.  In  such  case  the  electric  test  should  be  resorted  to.  (See 
Dry  Gangrene.)     In  some  cases  secondary  dentine  will  have  formed 

in  the  pulp  cavity  and  the  abscess  may  be 
found  in  one  of  the  filaments  while  the 
-^-'■•j  r'  -^ym^  other  will  be  apparently  healthy.     Fig. 

375  is  a  diagram  of   a  number  of  cases 
seen  in  practice. 

Prognosis.     General  experience  regards 
ulceration   and    abscess  of    the  pulp  as 
precursors   of    the  death  of   the  organ. 
Usually  this  is  by  progressive  suppura- 
Abscess  of  the  pulp  after  formation  ^^^^      j^  jg  Undoubtedly  truc,  howcver, 

of  a  large  amount  of  secondary  den-  .  . 

tine,  dividing  the  pulp  into  two  por-   that  attempts  at  circumvallatiou  of  the 

tions:  S  D,  secondary  dentine;   V  P,      -,        ■,    ,.  ■,      .  ^-r?' 

vital  pulp;  A  p,  abscess  or  confined   dead  tissuc  are  made  m  some  cases  (Fig. 

pus;   J,  area  of  apical  inflammation.     376),      The   pUS   Cclls    UudcrgO    dcgeUCra- 
(Diagrammatic. ) 

tion  and  the  abscess  site  may  be  the  seat 
of  calcareous  deposits.  Even  in  these  cases  death  is  delayed,  not 
averted.  The  remainder  of  the  pulp  undergoes  atrophic  changes,  and 
commonly  suppuration  reappears. 

Treatment.  The  treatment  of  the  case  consists  in  relieving  the 
existing  pain,  completing  the  devitalization  of  the  pulp,  and  removing 
it  in  such  a  manner  that  no  organisms  or  dead  matter  are  carried  beyond 
the  apex  of  the  root. 

To  secure  relief,  evacuation  of  the  pus  is  imperatively  necessary. 
The  organ  is  freely  exposed,  exercising  no  pressure  in  gaining  free 
access  to  it.  If  pus  do  not  flow  upon  exposure  of  the  surface 
of  the  pulp,  a  sharp,  slender,  sterilized  probe  is  quickly  passed  into 
the  substance  of  the  pulp,  when,  if  pus  be  present,  it  will  usually 
escape  freely  through  the  opening  thus  made  and  be  followed  by 
blood. 

If  the  pus  formation  be;  limited  and  circumscribed,  throbbing  pain 
may  follow,  which  promptly  quiets  under  an  application  of  cocaine  in 
glycerin.  The  application  is  not  made  until  the  pus  flow  ceases.  A 
pellet  of  cotton  wet  with  a  3  per  cent,  solution  of  formalin,  or  a  satu- 
rated solution  of  thymol,  is  laid  upon  the  pulp  and  the  cavity  is  sealed 
for  twenty-four  hours  (never  longer),  and  then  an  arsenical  application 


SUPPURATION  OF  THE  PULP. 


409 


is  made.  Should  the  exposed  portion  of  the  pulp  be  insensitive  it  is 
burred  away  until  access  is  had  to  the  vital  portion,  where  the  arsenic 
is  to  be  applied.     The  pulp  may  otherwise  be  surgically  removed. 


Fig.  376. 


Chronic  suppurative  pulpitis  terminating  in  calcification  of  the  pus  and  atrophy  of  the  pulp. 
A^,  larger  abscess,  filled  with  calcified  pus;  A^,  abscess  at  the  periphery  of  the  pulp;  A^,  A^, 
small  longitudinal  abscesses,  all  calcified;  N,  calcified  nerve  bundle;  C,  C,  calcareous  depo- 
sitions in  the  fibrous  pulp  tissue;  P,  P,  pigment  clusters  from  previous  hemorrhage.  X  10. 
(Bodecker.) 


The  rubber-dam  need  not  necessarily  be  applied  for  the  treatment 
preliminary  to  devitalization,  but  the  pulp  should  be  kept  under  the 
influence  of  antiseptics 


410 


DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 


CHRONIC  INFLAMMATION  OF  THE  PULP. 

In  cases  in  which  the  resistive  force  of  the  pulp  is  great  and  the 
causes  of  less  violent  nature  or  less  violent  in  action,  the  inflammation 
may  be  of  low  grade  and  continue  for  some  time.  Pulp  ulceration 
may  pursue  a  chronic  course,  as  has  already  been  described.  Abscess 
of  the  pulp  may  also  become  chronic,  and  the  pulp  may  even  encapsule 
the  pus  area  and,  the  bacteria  dying,  the  abscess  area  may  become 
the  seat  of  calcareous  deposits. 

Sclerosis  of  the  Pulp.  Inflammation  of  a  low  grade  may  persist 
in  the  pulp  for  long  periods,  giving  rise  to  an  increase  of  its  fibrous 
tissue  with  atrophy  of  the  cellular  elements,  producing  a  condition 
found  in  chronic  interstitial  inflammation  in  some  other  tissues — a 
sclerosis.  Instead  of  the  usual  distribution  of  myxomatous  tissue, 
bands   and   bundles   of  fibrous  tissue  appear.      The  pulp  appears 

Fig.  377. 


^^i/k^t^p^jf^m 


Chronic  inflammation  of  the  pulp,  areolation,  and  degeneration.     (Black,) 

shrunken  and  stiff,  bloodvessels  are  contracted,  and  the  nerve  fibres 
have  undergone  partial  or  complete  atrophy. 

Black  found  that  in  the  late  stages  of  sclerotic  atrophy  areolae 
developed  in  the  bundles  of  connective  tissue,  the  inflammatory 
elements  having  disappeared  and  the  areolae  being  occupied  by  fluid. 
Arkovy  describes  the  condition  as  reticular  atrophy  of  the  pulp 
(Fig.  377).  _  ^ 

The  condition  would  point,  as  suggested  by  Black,  to  venous  hyper- 
semia  as  the  cause  of  the  oedema  rather  than  inflammation;  but  the 
evidences  of  former  chronic  inflammation  in  the  existence  of  the 
bundles  of  reticulated  tissue  show  this  to  have  been  the  essential  con- 
dition. The  observations  of  the  same  writer  indicate  that  atrophy  of 
the  odontoblasts  is  a  usual  accompaniment  of  all  of  the  chronic  pulp 
affections. 


CHRONIC  INFLAMMATION  OF  THE  PULP. 


411 


Sclerotic  and  other  chronic  degenerations  of  the  pulp  usually  present 
the  history  of  one  or  more  attacks  of  pulpitis  in  the  past,  with  more 
or  less  continuous  uneasiness  extending  over  a  long  period.  The 
response  of  the  pulp  to  all  tests  becomes  diminished  and  dull. 

Treatment.     Such  pulps  are  to  be  devitalized  and  removed. 

Chronic  Hypertrophic  Pulpitis.  When  the  pulp  is  exposed  over  a 
wide  area,  long-continued  chronic  inflammation  may  lead  to  an 
enlargement  of  the  organ  with  a  protrusion  of  altered  pulp  mass 


Fig.  378. 


A,  a  first  lower  molar  with  a  cavity  at  a  completely  filled  by  a  hypertrophy  of  the  pulp,  which 
has  grown  out  through  the  orifice,  exposing  the  pulp  at  b.  B,  a  field  illustrating  the  tissue  of 
the  growth,  which  is  composed  almost  entirely  of  granulation  tissue  of  a  very  primitive  type : 
a,  a  covering  of  epithelium  presenting  papillse;  6,  epithelium  apparently  without  papillae. 
{Black.) 

through  the  orifice  of  exposure,  producing  the  condition  known 
clinically  as  fungous  pulp.  When  the  growth  extends  beyond  the 
boundaries  of  the  orifice  and  then  increases  in  bulk  it  forms  a  pedun- 
culated mass  to  which  the  term  polypus  of  the  pulp  has  been  applied. 
Morbid  Anatomy  and  Pathology.  The  growth  has  its  origin  in  a 
chronic  inflammation  of  the  body  of  the  pulp;  the  organ  swells,  and 
contact  with  the  sharp  edges  of  the  orifice  of  exposure  excites  a  con- 
tinued irritation,  leading  to  further  proliferation  of  the  cells  of  the 


412 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


inflamed  part,  so  that  a  large  mass  of  embryonic  tissue  is  formed 
(Fig.  378),  termed  by  Black  granulation  tissue  of  a  low  type.  As  in 
the  granulation  tissue  of  repair,  bloodvessels  grow  into  this  mass, 
so  that  it  may  bleed  at  a  slight  touch.  Black  noted  in  his  case 
illustrated  a  covering  of  squamous  epithelium  upon  the  periphery 
of  the  growth,  which  might  be  interpreted  as  the  transformation  of 


Fig.  379. 


Hyperplastic  myxomatous  pulp,  which  filled  a  carious  cavity :  if,  lobules  made  up  of  papillsfr 
of  a  myxomatous  structure,  rich  in  capillary  and  venous  bloodvessels;  6,  calcareous  globule  ; 
E,  epithelial  cover  of  papillse.     X  10.     (Bodecker.) 

mesoblastic  into  epiblastic  tissue,  but  the  correct  explanation  beyond 
doubt  is  that  advanced  by  the  same  author,  that  the  epithelium  is 
transplanted  from  the  gums,  and  grows  after  the  manner  of  a  skin- 
graft.    The  growth  does  not  contain  nerves. 

These  growths  may  undergo  further  changes;  higher  organization  of 
the  granulation  tissue  occurs  and  fibrous  tissue  is  formed ;  the  cells  may 


CHRONIC  INFLAMMATION  OF  THE  PULP. 


413 


undergo  degenerations,  first  granular,  then  fatty,  and  suppuration  and 
gangrene  may  occur.  Tomes^  records  a  case  where  calcification  of  a 
hypertrophied  section  of  a  pulp  occurred;  but  as  the  case  was  due  to 
traumatism  (fracture  of  a  tooth),  different  vital  conditions  existed  from 
those  in  the  cases  under  discussion.  Actual  calcification  of  the  mass 
is  scarcely  possible,  although  calcareous  degeneration  may  occur 
within  the  fungous  mass  (Fig.  379). 

Resorption   of  the   walls   of  the   pulp  chamber  may  occur  as  an 
accompaniment  of  chronic  pulpitis.    What  appears  to  be  an  idiopathic 


Fig.  380. 


Acute  pulpitis :  S,  secondary  dentine ;  B,  bay-like  excavations  filled  with  medullary  or  inflam- 
matory corpuscles;  V,  transverse  section  of  a  bloodvessel;  M,  multinuclear  body.  X  300. 
(Bodecker.) 

dentine  resorption  is  described  on  page  397.  Black  records  a  case 
where,  after  pulp  capping  in  a  lower  molar  and  the  insertion  of  a  large 
gold  filling,  the  tooth  was  examined  at  the  end  of  ten  years;  for  two  or 
three  years  the  pulp  had  given  evidences  of  irritability,  and  when  the 
pulp  was  removed  the  pulp  chamber  was  found  enormously  enlarged 
and  opening  into  the  pericementum  between  the  roots  of  the  teeth. 
Fig.  380  exhibits  resorption  of  previously  formed  secondary  dentine 
with  the  probable  agency  through  which  the  resorption  is  brought 


1  Dental  Sui-gery,  third  edition. 


414 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 


about.  The  area  of  resorption  is  invaded  by  numerous  multinucleated 
cells,  which  are  evidently  performing  the  function  of  odontoclasts. 

As  shown  by  Miller,  Hopewell-Smith,  and  others,  a  reconstructive 
change  may  occur  and  adventitious  dentine  be  redeposited  in  the 
area  of  resorption  (Fig.  365). 

Symptoms.  The  symptoms  of  chronic  pulp  inflammations  and 
degenerations  are  usually  those  of  long-continued  discomfort,  with 
reflex  pains,  which  rarely  persist  into  the  latest  stages  of  degeneration. 


Fig.  382. 


Fig.  383. 


Fig.  384. 


Hypertrophy  of  pulps.     (Garretson.) 

The  response  to  heat  and  cold,  present  at  first,  declines  until  the  pulp 
scarcely  reacts,  and  then  but  slowly. 

No  nerve  fibres  develop  in  the  hypertrophic  pulp  tissue,  so  that  the 
new-growth  has  no  sensitivity  in  itself,  although  pressure  upon  it  may 
cause  sharp  pain  through  the  still  vital  pulp  nerves  themselves. 

Four  or  five  of  these  hypertrophies  may  exist  in  a  mouth,  filling 
whole  cavities  of  decay,  the  surrounding  tooth  structure  being  in 

Fig.  385.  Fig.  386. 


Hypertrophy  of  the  pericementuin.    (Garretson.)  Hypertrophy  of  the  gum.    (Garretson.) 


various  stages  of  disintegration.  They  seem  to  be  comparatively 
insensitive  to  mastication  (Fig.  382). 

Hypertrophy  of  the  pulp  also  may  be  associated  with  pulp  ulcera- 
tion, the  growth  arising  from  one  canal  of  a  tooth. 

Regeneration  of  an  extirpated  pulp  has  been  claimed,  but  I  have 
never  seen  any  cases  that  were  not  referable  to  the  above  form  of 
hypertrophy  or  to  a  fungoid  growth  from  the  pericementum. 

Diagnosis.  The  only  condition  with  which  hypertrophic  pulp  may 
be  confounded  is  a  pedunculated  growth  of  gum  tissue  through  a 


CHRONIC  INFLAMMATION  OF  THE  PULP.  415 

cavity  at  the  neck  of  a  tooth  beneath  the  gum  margin  (Fig.  385).  It 
is  important  to  differentiate  between  these  conditions,  because  if  an 
apphcation  of  arsenical  paste  be  made  to  a  fungous  gum,  the  destruc- 
tion of  tissue  may  extend  into  the  sound  pericementum.  The  physical 
appearances  of  the  two  are  alike:  they  both  bleed  freely  and  have 
about  the  same  degree  of  sensitivity. 

Histological  examination  of  this  class  of  hypertrophy  of  the  gums, 
conducted  by  Dr.  Luigi  Ancone,'^  of  Italy,  demonstrated  that  the 
growth  is  a  simple  exaggeration  of  the  normal  elements  of  the  part. 

If  the  tumor  be  central  to  the  tooth  tissue  and  the  latter  not  decayed 
out  to  very  thin  walls,  it  may  be  at  times  laid  aside  by  means  of  a  blunt 
instrument  and  be  seen  to  have  its  origin  from  an  orifice  of  exposure 
(Fig.  381).  It  is  then  fairly  inferred  to  be  a  pulp  mass,  especially  if 
the  tooth  has  never  been  operated  upon.  The  diagnosis  may  be  a 
doubtful  one,  in  which  case  the  rubber-dam  is  to  be  applied,  the 
polypus  frozen  by  means  of  a  spray  of  ethyl  or  methyl  chloride,  and 
the  mass  removed  with  a  sharp  blade  passed  across  its  peduncle. 

The  source  of  the  tumor  may  then  be  usually  clearly  seen.  As  an 
alternative  proceeding  the  tissue  may  be  thoroughly  saturated  with  a 
strong  solution  of  trichloracetic  acid  and  then  ablated.  If  any  further 
doubt  exist  the  pulp  is  to  be  sterilized  with  hydrogen  dioxide,  etc.,  and  a 
pellet  of  cotton  saturated  with  oil  of  cloves,  carbolic  acid,  or  dental 
tincture  of  iodine  is  laid  upon  it,  and  over  this  temporary  stopping  is 
firmly  packed.  By  this  means  the  growth  may  be  pressed  away  until 
it  is  seen  to  arise  from  either  a  pulp  chamber  or  a  perforation  made 
by  decay  or  accidental  excavation  into  the  pericemental  tract. 

Pressure  anaesthesia  may  be  resorted  to  partly  as  a  diagnostic 
measure.  In  such  case  no  danger  exists  beyond  the  possible  forcing 
of  cocaine  into  the  gum  tissue.  Nervocidin  should  be  useful  in  cases 
of  doubt.    The  a;-rays  should  afford  a  diagnosis. 

Hemorrhage  may  be  checked  with  adrenalin  chloride  1  :  1000  solu- 
tion, or  25  per  cent,  pyrozone  or  a  saturated  solution  of  silver  nitrate. 

Treatment.  If  the  case  be  one  of  pulp  hypertrophy,  arsenic  may  be 
applied  or  pressure  anaesthesia  attempted  for  pulp  removal. 

Crystals  of  iodine  have  been  used  with  satisfaction  in  combination 
with  pressure  for  pulp  devitalization. 

If  a  perforation  exist  it  is  to  be  treated  by  sealing  the  orifice  with 
gutta-percha  or  copper  amalgam  if  practicable.  (See  Therapeutics  of 
Dental  Caries.) 

1  Abstract  from  rOdontologia  by  Dr.  W.  Dunn,  in  International  Dental  Journal,  1899. 


416 


DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 


Fibroid  Degeneration  of  the  Pulp.    Apart  from  the  degenerations 
due  to  inflammatory  conditions,  a  form  of  degeneration  occurs  "as  a 


Fig.  387. 


DO 


DO 


Horizontal  section  of  fibroid  degeneration  of  the  pulp  in  situ.  Prepared  by  Mr.  Hopewell- 
Smith's  process:  D,  deeply  stained-dentine ;  5,  large  areolar  spaces;  X*  0,  degenerate  odonto- 
blasts; P,  fibroid  tissue  of  pulp.     X  45.     (Hopewell-Smith.) 

natural  old-age  termination  of  the  life  of  a  healthy  pulp,"  and  similar 
to  senile  changes  occurring  in  the  pericementum.  (See  Fibroid  Degen- 
eration of  Pericementum.)    This  change,  first  described  by  Hopewell- 


DEGENERATION  OF  THE  PULP. 


417 


Smith/  occurs  in  teeth  of  the  aged  in  whose  mouths  simple  alveolar 
resorption  has  occurred. 

Morbid  Anatomy.  "  The  pulps  are  shrunken  and  may  have  left  the 
wall  of  the  pulp  chamber.  Many  areolar  spaces  appear  which  may 
be  arranged  in  chains.  The  odontoblasts  are  degenerated.  The  pulp 
stroma  is  very  dense,  has  a  clear,  fibrous  structure,  becomes  very 
marked  in  staining,  and  is  highly  differentiated  from  the  surrounding 


Fig.  388. 


Fibroid  degeneration  of  the  pulp.     D,  dentine  with  tubules  ;  FO,  fibroid  odontoblasts  ; 
P,  atrophied  pulp  tissue. 


tissue.  The  bloodvessels,  nerves,  cells,  and  connective  tissue  have  all 
disappeared  and  their  place  is  taken  by  a  new,  firm,  fibrous  structure 
devoid  of  cells,  nuclei,  or  any  regular  arrangement  of  constituent 
parts. 

''  There  is  no  calcification  of  the  pulp  and  no  obliteration  of  the 
dentinal  tubules. 

"  The  proximate  cause  and  associate  phenomena  are  not  as  yet 
clearly  related." 

1  Histology  and  Patho-histology  of  the  Teeth. 

27 


418  DESTRUCTIVE  DISEASES  OF  THE  DEXTAL  PULP. 

Fatty  Degeneration  of  the  Pulp.  During  the  course  of  degeneration 
of  the  elements  of  the  pulp  fatty  changes  may  occur  as  in  other  parts. 
The  fatty  changes  occur  in  the  walls  of  the  arteries  and  sheaths  of 
the  nerves,  and  in  the  odontoblasts.^ 

Practically  all  of  the  destructive  pulp  diseases  (excepting  sclerosis 
and  fibrosis)  occur  in.  the  pulps  of  the  temporary  teeth,  and  are  to  be 
treated  in  like  manner  except  as  to  the  use  of  arsenic,  which,  being 
accompanied  by  greater  danger,  should,  for  the  most  part,  be  replaced 
by  nervocidin,  pressure  anaesthesia,  or  cantharides.  This  point  is 
discussed  at  length  in  the  chapter  upon  removal  of  the  pulp. 

If  the  tooth  roots  be  largely  resorbed  the  pulp  may  bear  capping 
with  a  paste  composed  of  oxide  of  zinc  and  eugenol,  even  when  ulcer- 
ation has  occurred.  The  pulp  may  die  under  this  capping,  when  the 
case  is  further  treated  as  indicated.     (See  Chronic  Apical  Abscess.) 

1  Hopewell-Smith. 


CHAPTER    XVIII. 

METHODS  OF  EEMOVAL  OF  THE  DENTAL  PULP  AND 
EOOT-CANAL   FILLING. 

The  removal  of  the  dental  pulp  being  a  valued  and  in  some  cases 
the  only  method  of  curing  certain  pulp  diseases,  a  consideration  of 
the  methods  available  is  of  importance. 

1.  Under  the  influence  of  a  general  anaesthetic,  nitrous  oxide  or 
even  ether,  the  pulp  cavity  may  be  opened  and  the  pulp  removed. 
The  influence  of  nitrous  oxide  as  ordinarily  administered  will  be  too 
evanescent  to  permit  removal  of  root  filaments  of  pulps  of  multirooted 
teeth.  In  these,  therefore,  the  removal  of  the  pulp  bulb  alone  is,  as 
a  rule,  accomplished.  By  this  means  the  pulp  is  depleted  and  the 
engorgement  of  the  pulp  vessels  reduced.  The  devitalization  is 
completed  with  arsenic,  or  by  cocaine  pressure  or  nervocidin  anaesthesia. 

In  single-rooted  teeth  the  pulp  chamber  may  be  opened  with  a 
sharp  bur  and  the  pulp  quickly  removed  with  a  barbed  broach.  Under 
the  influence  of  ether  the  operation  may  be  made  complete  in  any 
tooth.    It  is  seldom  used  for  the  purpose. 

2.  Sprays  of  rapidly  vaporizable  substances,  such  as  ethyl  or  methyl 
chloride,  directed  against  the  exposed  pulp,  the  tooth  being  isolated 
under  rubber-dam,  will,  in  some  cases,  render  the  pulp  entirely  insen- 
sitive, although,  as  a  rule,  they  fail  to  entirely  anaesthetize  to  the  apical 
foramen.  The  method  is  painful  and  not  applicable  in  many  cases 
of  highly  irritable  pulps. 

3.  Applications  of  even  saturated  solutions  of  cocaine  being  ineffective, 
it  has  been  suggested  to  inject  cocaine  into  the  pulp:  the  surface  of 
the  pulp  is  benumbed  by  applications  of  strong  solutions  of  cocaine, 
the  needle  of  a  hypodermic  syringe  containing  a  solution  of  cocaine 
hydrochlorate  (from  4  per  cent,  to  10  per  cent.)  is  quickly  thrust  into 
the  pulp  canal,  and  a  drop  of  the  solution  forcibly  injected;  in  a  few 
seconds  the  pulp  may  be  so  benumbed  that  it  can  be  removed.^  This 
procedure,  however,  appears  to  fail  as  often  as  it  succeeds.  A  strong 
solution  of  silver  nitrate  has  been  suggested  by  Dr.  A.  N.  Gaylord  as 
useful  in  place  of  the  cocaine  before  applying  the  needle. 

1  Maxfield,  Proceedings  of  the  Xew  Jersey  State  Dental  Society,  1891. 


420     REMOVAL  OF  DEXTAL  PULP  AND  ROOT-CANAL  FILLING. 

4.  Cocaine  cataphoresis  is  usually  effective,  although  in  conditions  of 
active  hypersemia  and  inflammation  even  the  maximum  current  and 
saturated  solutions  of  the  alkaloid  may  fail  to  subdue  the  irritability 
of  the  pulp.  In  favorable  cases  about  fifteen  minutes  are  required 
for  pulp  anaesthesia. 

5.  A  more  reliable  method  of  utilizing  cocaine  is  in  combination  with 
pressure.  The  rubber-dam  is  applied.  A  small  pellet  of  amadou 
(spunk)  is  wet  with  a  saturated  solution  of  cocaine  hydrochlorate  in 
water,  alcohol,  or  chloroform,  and  then  dipped  in  the  finely  powdered 
cocaine.  It  is  then  laid  upon  the  pulp  and  a  strip  of  soft,  vulcanizable 
rubber  is  folded  into  the  cavity  until  it  fills  it.  X  burnisher  as  large 
as  convenient  is  then  used  to  gently  press  the  rubber  in  the  direction 
of  the  pulp.  A  piece  of  amadou  placed  over  the  rubber  will  concentrate 
the  force  of  the  burnisher  and  prevent  egress  of  the  rubber.  A  slight 
pain  will  be  produced,  upon  indication  of  which  further  pressure  should 
cease  for  the  time,  but  the  advance  made  be  maintained.  In  a  half- 
minute  pressure  may  be  again  renewed  and,  unless  pain  be  produced, 
be  increased  until  the  full  force  of  the  wrist  is  exerted.  The  rubber  and 
spunk  are  then  removed,  the  pulp  cavity  opened,  and  the  pulp  lifted 
away  with  a  broach.  For  multirooted  teeth  a  more  prolonged  pressure 
is  required  than  for  the  single-rooted.  On  account  of  possible  non- 
removal  of  some  portion  of  pulp  tissue  in  fine  roots  it  may  be  well 
to  instill  carbolic  acid  into  the  fine  canals  to  prevent  return  of  sensation. 
By  this  operation  the  pulp  tissue  is  \^sibly  compressed  and  in  some 
cases  ischsemia  with  its  accompanying  lessening  of  sensibility  is  pro- 
duced; at  the  same  time  the  cocaine  is  probably  forced  into  the  pulp 
tissue.  In  some  cases  the  anaesthesia  is  satisfactory,  while  the  pulp 
itself  still  bleeds  readily,  so  that  cocaine  anaesthesia  seems  the  most 
satisfactory  explanation.  The  operation  appears  to  fail  in  the  teeth 
with  very  large  foramina,  though  with  the  moderately  large  foramina 
it  is,  as  a  rule,  successful.  Some  pulps  rebel  totally  against  the  treat- 
ment, some  require  several  applications,  and  some  are  not  affected  at 
all  by  the  second  application.  The  application  sometimes  stops  acute 
pain  and  sometimes  produces  it  in  a  fairly  quiet  pulp.  In  all  these 
the  conditions  may  seem  favorable  to  the  attempt.  The  effect  seems 
most  pronounced  when  the  exposure  is  free  and  the  pressure  effected 
in  a  direct  line  with  the  pulp  axis.  For  this  reason  a  second  application 
may  be  successful  while  the  first  may  only  permit  a  better  exposure. 
The  dentine  may  be  anaesthetized  by  the  method  in  order  to  gain  an 
exposure  in  cases  of  sound  teeth  from  which  it  is  desired  to  remove 


REMOVAL  OF  DENTAL  PULP  AXD  ROOT-CANAL  FILLING.      421 

pulps  by  this  method.  In  some  cases  it  is  necessary  to  close  the  buccal 
and  lingual  interdental  openings  by  means  of  the  thumb  and  forefinger 
in  order  to  concentrate  the  force  exerted  upon  the  pulp.  The  force 
should  be  carefully  applied  in  cases  of  frail  walls.  These  are  perhaps 
better  cut  away.  In  cases  of  ulcerated  pulp  filaments  the  above- 
described  pressure  may  be  modified.  A  thread  of  spunk  may  be 
saturated  with  carbolic  acid  or  carbolic  acid  and  cocaine  and  packed 
into  contact  with  the  pulp  and  the  pressure  with  vulcanite  rubber 
made.  Some  caution  should  be  observed  in  the  use  of  both  cataphoresis 
and  pressure  anaesthesia  after  partial  devitalization  by  the  use  of 
arsenic,  as  cases  have  been  recorded  of  the  carriage  of  the  latter  to 
the  apical  tissues  by  these  means.  The  obvious  indication  is  the 
thorough  removal  of  all  arsenic  and  dead  tissue  before  applying  either 
of  the  cocaine  methods.  Cases  of  the  systemic  action  of  cocaine  via  the 
pulp  have  been  noted  in  this  method.  Some  of  these  cases  are  due  to 
syncope  alone,  as  it  has  occurred  when  other  materials  have  been  used 
experimentally.  Hemorrhage  after  the  pulp  extraction  may  be  treated 
with  adrenalin  chloride,  1 :  1000,  caustic  pyrozone,  zinc  chloride,  or 
other  styptic. 

6.  Arkovy  has  recommended  nervocidin  for  its  anaesthetic  action 
upon  the  pulp.  A  small  quantity  is  placed  upon  a  piece  of  spunk  and 
applied  to  the  pulp,  which  it  anaesthetizes  in  from  a  few  hours  to  a  day, 
when  the  pulp  may  be  painlessly  removed  in  an  ischsemic  condition. 
Two  applications  are  required  in  case  of  unexposed  pulp:  one  to 
obtain  a  painless  exposure.^    It  is  not  injurious  to  the  gum. 

7.  A  fully  exposed  pulp  in  a  single-rooted  tooth  or  single  root  of  a 
multirooted  tooth  may  be  suddenly  "knocked  out"  by  means  of  a 
delicately  pointed  orange-wood  stick  or  Portuguese  tooth-pick.  The 
point  is  dipped  in  carbolic  acid,  and  suddenly  and  boldly  driven  into 
the  pulp  either  by  hand  or  mallet  force.  The  method  is  not  so 
agreeably  delicate  as  pressure  anaesthesia. 

8.  Darby  uses  with  success  in  deciduous  teeth  a  paste  of  about 
Yo  grain  of  cantharides  in  carbolic  acid.  The  application  must  be 
very  carefully  sealed.  Flagg^  has  mentioned  a  case  of  strangury  in  a 
man  as  the  result  of  its  use  against  a  tooth  pulp.  While  probably  an 
idiosyncratic  case,  the  effect  is  in  correspondence  with  the  known 
occasional  effect  of  cantharides  applied  as  a  vesicant. 

9.  A  vital  remnant  of  pulp  may  be  removed  after  instilling  carbolic 
acid  or  a  paste  of  carbolic  acid  and  acetate  of  morphine  into  its  sub- 

1  Soderberg,  Dental  Cosmos,  1901  and  1902.  2  Private  communication. 


422     REMOVAL  OF  DEXTAL  PULP  AXD  ROOT-CANAL  FILLING. 

stance  by  means  of  a  ''puncture  probe."  This  instrument  may  be 
made  by  filing  down  an  old  Donaldson  cleanser  to  a  fine  point,  which 
is  further  whetted  on  an  oil  stone.  The  sides  of  the  probe  are  polished 
by  folding  a  cuttle-fish  disk  upon  itself,  holding  it  between  the  thumb 
and  forefinger  of  the  left  hand  and  drawing  the  probe  through  it. 
The  pulp  canal  is  flooded  with  the  carbolic  acid  and  gentle  thrusts 
are  made  into  the  pulp  until  the  probe  is  stopped  at  the  apex.  If  it 
pass  through,  that  must  be  judged  by  the  sense  of  touch.  At  times  a 
small  end  of  pulp  filament  may  be  seared  with  a  hot  Evans'  root  drier 
which  is  quickly  thrust  into  it.  This  does  not  necessarily  give  much 
pain. 

10.  A  slow  but  effective  method  of  disposing  of  these  filaments, 
when  hyperirritable  or  when  patients  are  timid,  consists  in  packing  a 
cotton  twist  saturated  with  carbolic  acid  containing  cocaine  hydro- 
chlorate  in  solution  into  contact  with  the  pulp  and  then  gently  com- 
pressing the  pulp.  The  cotton  is  to  be  left  in  position  for  a  day  or 
two,  when,  as  a  rule,  the  pulp  may  be  removed. 

11.  Arsenious  acid  (arsenic  trioxide)  is,  as  a  rule,  prompt,  certain, 
and  complete  in  its  action,  and  is  applicable  for  de^dtalization  in  nearly 
all  cases  of  pulps  in  mature  teeth.  It  was  introduced  by  Spooner  for 
this  purpose  in  1836. 

When  a  small  quantity  of  pure  powdered  arsenic,  or  of  a  paste  in 
which  it  is  mixed  with  other  ingredients,  is  applied  to  the  pulp  horn 
or  the  dentine,  the  pulp  gradually  dies  progressively  from  the  horn 
toward  the  apex.  So  universally  is  this  the  case  that  a  short  application 
almost  invariably  involves  the  necessity  of  a  second  application  to  the 
pulp  or  of  a  painful  extirpation  of  the  undevitalized  portion  of  pulp. 

Action  of  Arsenic  upon  the  Pulp. — i^rkovy^  was  the  first  to  point  out 
the  details  of  the  action  of  arsenic  upon  the  dental  tissues: 

"1.  AS2O3  brought  into  contact  with  the  tooth  pulp  acts  in  the 
following  way:  a  certain  degree  of  inflammatory  hypersemia,  total  or 
partial,  depending  upon  the  quantity  of  the  agent  applied,  sets  in; 
the  bloodvessels  become  expanded,  and  here  have  a  tendency  to 
thrombosis.  This  latter  effect  may  also  be  in  connection  with  embolism 
of  the  capillaries,  when  the  agent  is  quickly  taken  up  into  the  blood- 
vessels. 

"2.  AS2O3  produces  no  coagulation  of  tissue  whatever. 

"3.  It  has  a  specific  influence  upon  the  blood  corpuscles,  combining 
with  the  haemoglobin  to  form  a  compound  of  arsen-hsemoglobin,  and 

I  Transactions  of  the  International  Medical  Congress,  London,  1881. 


ACTION  OF  ARSENIC  UPON  THE  PULP.  42a 

of  this  chemical  process  there  seems  to  be  evidence  in  the  profuse 
yellowish  tinge  of  the  whole  pulp  tissue  and  in  the  discoloration  of 
blood  in  several  of  the  bloodvessels. 

"4.  In  nearly  every  case  it  is  taken  up  in  substantia  (in  form  of 
molecules)  into  the  blood-ways;  when  there  it  produces,  besides  the 
above-mentioned  changes,  granular  detritus  of  the  contents  and  anaemic 
collapse — shrinkage,  the  latter  effect  being  brought  about  nearly 
exclusively  in  cases  where  greater  doses  were  used. 

"5.  The  bulk  of  the  pulp  tissue — viz.,  connective-tissue  fibres  and 
odontoblasts — undergoes  no  change  whatever;  not  so  the  connective- 
tissue  cells,  which  increase  three  or  four  times  their  normal  size. 

"6.  The  special  action  of  arsenic  trioxide  upon  the  nerve  elements 
consists  in  the  following :  the  neurilemma  is  only  so  far  influenced  that 
its  nuclei  are  somewhat  increased;  a  more  essential  change  takes  place 
in  the  axial  part,  where,  after  the  application  of  more  than  one  mgrm., 
granular  destruction  of  myelin  sets  in,  and  the  axis-cylinder  commences 
here  and  there  to  disappear.  A  very  surprising  alteration  may  be  seen 
in  the  notchy  tumefaction  of  the  axis-cylinder,  described  heretofore 
almost  only  in  cases  of  central  lesions. 

"7.  All  these  alterations  occur  in  and  among  normal-looking 
tissue. 

"8.  The  action  of  arsenic  trioxide  is  macroscopically  exhibited  by  a 
brownish-red  tingeing  of  the  whole  or  of  certain  parts  of  the  pulp 
body,  as  well  as  of  the  neighboring  dentine  and  the  cementum,  this 
latter  in  cases  treated  with  greater  doses — viz.,  two  to  five  mgrms. 
This  alteration  is  most  expressed  at  the  top  of  the  crown  pulp  and  at 
the  apical  one-fourth  to  one-third  part.  This  circumstance  may  be 
considered  as  an  external  evidence  of  the  devitalization  being  com- 
pletely attained  to." 

In  some  cases  the  pinkish  discoloration  of  the  dentine  may  be 
marked;  the  broken-down  corpuscles  of  the  extravasated  blood  have 
their  coloring  matter  taken  up  by  the  odontoblasts,  and  being  dis- 
tributed through  their  protoplasmic  processes  produce  a  condition 
technically  known  as  suffusion.  The  same  result  may  be  an  attendant 
upon  injury  to  the  vessels  from  other  causes,  from  sudden  thrombosis, 
as  when  teeth  are  moved  too  rapidly  in  regulating. 

Miller's  experiments^  upon  the  tails  of  mice  (made  without  and  with 
rings  at  the  root  of  the  tail  to  simulate  the  surroundings  of  the  apical 
vessels  of  a  tooth;  made  without  and  with  encasement  of  the  tails  in 

1  Dental  Cosmos,  1894. 


424     REMOVAL  OF  DEXTAL  PULP  ASD  ROOT-CAXAL  FILLIXG. 

plaster  of  Paris  to  imitate  the  rigid  surroundings  of  the  dental  pulp) 
showed  that  in  the  absence  of  the  plaster  encasement  enormous  oedema 
of  the  tail  was  produced  and  a  sensory  paralysis  of  the  hind  limbs; 
complete  ansesthesia  of  the  tail  occurred  in  forty-eight  hours.  "  The 
action  of  arsenic  appeared  somewhat  accelerated  when  a  glass  ring 
was  applied  close  to  the  root  of  the  tail.  In  more  than  forty  cases 
there  was  not  one  in  which  the  action  of  the  arsenic  extended  beyond 
the  ring,  and  the  action  was  not  appreciably  affected  by  enclosing  the 
tails  in  plaster  casts.  The  action  of  the  arsenic  is  of  a  progressive 
nature,  beginning  at  the  point  of  application  and  extending  gradually 
in  each  direction." 

Flagg^  devitalized  ten  pulps  and  removed  them,  cut  off  the  portion 
of  the  bulb  of  each  which  had  contact  with  the  arsenic,  and  tested  the 
ten  pulps  together  by  Reinchs'  test.  Arsenic  was  found,  estimated  at 
a  one-hundred-thousandth  part  of  a  grain  or  one-millionth  of  a  grain 
for  each  pulp.  Allowing  for  possible  mechanical  introduction  or 
contact  of  arsenic  during  extirpation,  the  quantity  of  arsenic  introduced 
by  the  circulation  must  be  very  minute  indeed. 

Flagg  argued  that  as  the  pulp  subsequently  putrefies  it  cannot  have 
died  as  the  result  of  arsenical  poisoning  alone. 

The  indication  is  that  a  minute  quantity  of  arsenic  is  absorbed, 
exerts  its  peculiar  chemical  effects,  which  cause  the  pulp  in  part  to 
become  quickly  filled  with  blood.  Circulation  in  the  part  ceases  and 
death  of  the  part  ensues.  Arkdvy's  and  Miller's  experiments  seem  to 
show  that  the  arsenic  may  be  absorbed  into  part  of  the  pulp  beyond 
the  original  area  of  congestion,  and  this  probably  produces  further 
stasis,  which  progresses  apexward.  It  has  been  contended  that  arsenic 
may  pass  out  through  the  apical  foramen.  For  the  roots  with  large 
foramina  this  has  been  shown  to  be  true,  as  areas  of  devitalization  of 
the  apical  and  overling  gum  tissue  have  been  noted.  In  several  appar- 
ently authentic  cases  the  pericementum  of  a  mature  tooth  has  been 
said  to  be  destroyed  from  the  apex  down  and  the  tooth  lost.  I  have 
never  seen  such  a  case  resulting  from  the  arsenical  method  alone  in 
either  clinical  or  private  practice,  though  cases  of  marginal  gum 
alveolar  and  pericemental  death  beginning  as  the  result  of  leakage 
or  application  to  perforations  have  been  noted.  It  is  probable  that  as 
stasis  proceeds  the  apical  portion  of  the  pulp  becomes  involved  in 
advance  of  arsenic  absorption.  Miller's  experiments  show  that  arsenic 
does  not  pass  the  point  of  constriction. 

1  Dental  Cosmos,  1868. 


VARIATIONS  IN  THE  ACTION  OF  ARSENIC.  425 

Variations  in  the  Action  of  Arsenic.  In  most  cases  of  fully  formed 
single-rooted  teeth  in  young  adults,  an  application  of  arsenical  paste 
directly  to  the  exposed  pulp  will  be  followed  by  the  complete  death  of 
the  organ  in  forty-eight  hours.  At  the  expiration  of  that  time  a  steril- 
ized broach  may  be  passed  almost  to  the  apex  of  the  root  and  the  pulp 
removed  en  masse  without  pain.  Pulps  of  molars  require  a  longer 
time,  often  a  week,  before  the  filaments  are  dead.  The  finer  filaments 
resist  longer  than  the  larger  ones.  If  pulp  nodules  exist,  the  action  of 
the  arsenic  may  be  delayed  or  in  some  cases  be  almost  nil.  In  calcareous 
and  other  chronic  pulp  degenerations  the  action  is  also  delayed.  If 
arsenical  applications  are  made  over  a  layer  of  dentine,  the  same 
delay  is  noted,  and  is  increased  in  very  mature  teeth.  There  is  also 
a  greater  tendency  to  suffusion. 

Some  pulp,  irrespective  of  the  pulp  condition,  exhibits  a  peculiar 
idiosyncrasy  in  resisting  the  action  of  arsenic,  requiring  large  doses  and 
long  applications  before  succumbing. 

Forms  in  which  Used.  The  following  formulae  have  been  recom- 
mended. The  analgesics  included  are  intended  to  dilute  the  arsenic 
and  quiet  the  pulp  and  thus  both  directly  and  indirectly  modify  the 
pain: 


1. 

1^ — Acidi  arsenosi, 

Morphinfe  sulph., 

da 

gr.  X. 

Acidi  carbolici, 

q.  s.  ft.  pasta.— M. 
(J.  D.White.) 

2. 

9^ — Acidi  arsenosi, 

gr.  X. 

Morphinae  acetatis, 

gr.  XX. 

Olei  caryophylli, 

q.  s.  ft.  pasta.— M. 

Creosote  may  be  substituted  for  oil  of  cloves. 

(J.  Foster  Flagg.) 

3. 

9* — Acidi  arsenosi, 

gr.  X. 

Cocainse  liydrocli., 

gr.  XX. 

Olei  einnamonii. 

q.  s.  ft.  pasta.— M. 
(E.  0.  Kirk.) 

4.  Any  of  the  above  may  have  the  powdered  ingredients  mixed. 
The  cotton  pellet  may  be  wet  with  an  analgesic  oil  and  then  dipped 
into  the  powder. 

5.  Absorbent  cotton  cross  cut  with  scissors  to  a  fine  lint  may  be 
dusted  into  any  of  the  above  pastes  made  thin  by  adding  an  extra 
portion  of  the  menstruum.    It  is  then  dried  and  bottled  for  use.^ 

As  the  ordinary  pastes  tend  to  separate  into  layers  of  arsenic, 
morphine,  and  menstruum  if  made  thin,  they  should  either  be  made 
into  stiff  pastes  or  spread  over  the  bottom  of  a  wide  jar  so  that  some 
arsenic  may  be  scraped  off  the  bottom  at  each  application. 


1  J.  Foster  Flag 


426     BEMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING. 

Miller  suggests  using  thymol  in  connection  with  arsenic,  it  being 
both  analgesic  and  antiseptic.  He  offers  the  following  general  rules 
as  deductions  from  his  observations: 

"  1 .  The  rapidity  and  intensity  of  the  action  of  arsenious  acid  depend, 
under  certain  circumstances,  to  a  very  considerable  degree  upon  the 
substance  or  substances  with  which  it  is  incorporated. 

"  2.  Where  there  is  but  a  small  point  of  exposure,  and  in  particular 
where  extensive  calcification  has  taken  place  in  the  pulp,  escharotics 
should  be  avoided,  since  the  coagulation  of  the  tissue  retards  the 
absorption  of  the  arsenic.  This  retardation  is  but  slight  where  there 
is  a  broad  surface  of  exposure.  In  stubborn  cases,  where  applications 
of  the  ordinary  paste  fail  to  effect  the  devitalization,  a  paste  consisting 
of  arsenious  acid  in  oil  of  cloves,  glycerin,  or  salt  solution  should  be 
employed,  undiluted  by  any  third  constituent. 

"3.  Thymol  is  worthy  of  a  trial  as  a  substitute  for  morphine,  on 
account  of  its  anaesthetic  and  antiseptic  properties. 

"  4.  For  devitalizing  pulps  of  temporary  teeth  or  remains  of  pulp 
tissue  in  root  canals,  arsenious  acid,  if  employed  at  all,  should  be 
diluted  with  two  or  three  parts  of  some  other  constituent  (thymol,  zinc 
oxide,  morphine,  iodoform)." 

Cobalt  was  introduced  by  Robert  Arthur  as  a  devitalizing  agent 
some  forty  years  ago.  Within  recent  years  it  has  been  employed, 
notably  by  the  Herbst  method  (which  see),  to  destroy  pulps.  The 
cobalt  paste  of  Herbst  was  analyzed  by  E.  C.  Kirk  and  found  to 
consist  of  metallic  arsenic  and  cocaine  hydrochlorate.  Kirk  suggests 
that  free  acids  which  cocaine  salts  may  contain,  or  the  chlorine  from 
the  chloride,  may  combine  with  the  metallic  arsenic  and  form  soluble 
salts.  Commercial  cobalt  will  certainly  devitalize  the  dental  pulp, 
but  it  is  in  consequence  of  the  arsenic  contained  in  it. 

Mode  of  Application.  After  sterilization  of  the  cavity  and  pulp  and 
drying,  a  minute  pellet  of  cotton  is  to  be  rolled  in  the  paste  and  placed 
in  the  desired  location.  As  arsenic  destroys  gum  tissue  freely  it 
should  be  used  in  minute  quantity  only  and  be  accurately  sealed  in 
the  cavity. 

In  purely  occlusal  cavities  the  application  may  be  covered  with  a 
flat  pellet  of  cotton  containing  an  analgesic  and  over  this  temporary 
stopping  or  cement  may  be  placed.  In  those  cases  in  which  the 
cervical  wall  approaches  the  gum  the  rubber-dam  should  be  applied, 
the  cavity  dried,  and  temporary  stopping  packed  against  the  cervical 
wall,  allowing  it  to  extend  against  the  adjoining  tooth.    Other  portions 


APPLICATION  OF  ARSENIC.  427 

are  packed  into  the  buccal  and  lingual  walls.  A  pocket  is  thus  formed 
into  which  arsenic  may  be  safely  placed  and  covered  with  a  pellet  of 
cotton  containing  an  analgesic;  over  this  may  be  placed  a  last  pellet 
of  temporary  stopping  which  closes  the  opening.  When  one  is  expert 
the  dam  may  at  times  be  dispensed  with. 

If  the  packing  of  the  temporary  stopping  upon  the  pulp  be  feared 
a  small  pellet  of  amadou  may  be  laid  over  the  exposure,  and  after  the 
stopping  is  placed  it  may  be  removed. 

The  same  principle  may  be  employed  with  Flagg's  "facing" 
amalgam  or  its  equivalent  (alloy — silver,  40  parts;  tin,  55  parts;  zinc, 
5  parts  plus  mercury). 

It  may  be  used  in  desperate  cases  in  which  no  great  retaining 
periphery  exists  or  where  displacement  by  mastication  is  feared.  In 
its  use  a  pellet  of  spunk  is  laid  upon  the  pulp  and  the  cavity  is  practi- 
cally filled  with  the  soft  amalgam.  An  excavator  is  then  used  to  cut 
through  to  the  spunk,  which  is  carefully  withdrawn.  An  opening  is 
thus  left  into  which  the  application  and  the 

11  1-11  1  ^i'^-  389. 

extra  cotton  pellet  saturated  with  the  anal- 
gesic is  placed.  The  opening  is  then  dried 
and  sealed  with  a  portion  of  amalgam.  This 
amalgam  will  retain  its  integrity  for  months, 
yet  may  be  removed  in  a  few  minutes  by 
dividing  the  filling  into  two  portions. 
When  pulp  removal  is  intended  the  ap- 

„T       ,•  1  1      .1  1       J.1  Diagram  showing  method  of  first 

plication      may     be     removed      through     the     making  the  covering  for  an  arseni- 

opening  and  a  probe  may  be  passed  into   ^ai  or  sedative  application.    (See 

^  ^  ,  f>      1  1       •       ^^^^■)    E  P,  exposed  pulp;  A  A,  ar- 

the    pulp    to    test   the    progress    of    the    aew-    senioal    application;     C,    sedative 

talization.     If  needed,  a  second  application  "^"^^  f  ^"f^^  =  ^'  "'"^!^"°! 

'  i:  i:  placed  before  these   applications; 

may  be  made  or  the  tooth  may  be  tempo-  a',  amalgam  to  seal  them  in;  e, 
rarily  closed.   In  case  the  pulp  be  found  par- 
tially dead  it  is  better  to  allow  more  time  for  complete  devitalization 
than  to  make  a  second  application  (Fig.  389) . 

Adhesive  zinc  phosphate  may  be  flowed  over  an  application  if  the 
cavity  be  accessible  and  gravity  be  not  likely  to  interfere.  The  saliva 
may  be  admitted  as  soon  as  the  cement  begins  to  stiffen. 

The  chief  objection  to  the  placing  of  coverings  aper  the  application 
has  been  made  is  the  danger  of  squeezing  the  arsenical  paste,  which 
causes  capillary  attraction  to  quickly  carry  the  arsenic  to  the  cervical 
gum  tissue. 

If  redundant  gum  be  within  the  cavity  of  decay  it  is  to  be  carefully 


428     REMOVAL  OF  DEXTAL  PULP  AXD  ROOT-CAXAL  FILLIXG. 

saturated  with  trichloracetic  acid  and  cut  away  before  attempting  to 
make  the  arsenical  preparation.  It  has  been  recommended  that 
carbolic  acid  be  always  applied  to  the  gum  margin  to  kill  it.  It  is 
argued  that  arsenic  will  not  pass  through  dead  tissue.^  It  is  better, 
however,  that  no  confusion  of  diagnosis  occur.  If,  after  an  application 
is  made,  dead  gum  be  found,  it  is  to  be  presumed  to  have  been  caused 
by  the  arsenic  and  treated  accordingly.  If  the  coverings  be  made  as 
suggested  the  danger  of  leakage  is  greatly  lessened. 

If  the  cavity  be  inaccessible,  and  the  rubber-dam  cannot  be  used 
to  exclude  fluids,  and  an  arsenical  application  cannot  be  made  with 
precision,  or  when  arsenic  applied  directly  is  likely  to  cause  pain,  it  is 
advisable  to  form  a  special  cavity  or  "  pocket  "^  for  its  reception.  This 
should  always  be  made  when  possible  in  a  line  of  direct  approach  to 
a  healthy  pulp  horn.  The  cavity  is  to  be  made  as  deep  as  possible 
without  plunging  into  the  pulp.  A  spear  drill  of  narrow  face  is  to  be 
used.  As  a  rule,  in  the  conditions  demanding  extirpation  of  the  pulp 
the  dentine  is  insensitive  or  nearly  so,  so  that  the  pulp  may  be  almost 
exposed  without  pain.  An  exception  to  this,  however,  is  found  when 
pulp  nodules  exist,  when  the  dentine  may  be  exquisitely  sensitive.  In 
these  cases  two  or  more  applications  of  the  paste  are  required;  as  soon 
as  the  pulp  can  be  exposed,  a  direct  application  of  the  paste  is  to  be 
made.  The  cavity  of  decay  is  used  as  a  receptacle  for  analgesics  in 
these  cases. 

Cervical  cavities  not  ha"s^ng  a  retentive  form,  and  abraded  teeth, 
offer  difficulties,  which  are  overcome  by  drilling  a  pocket  for  the 
reception  of  the  paste. 

In  cases  where  there  are  pulp  nodules,  and  where  chronic  degen- 
erations of  the  pulp  exist,  the  arsenic  is  removed  at  the  end  of  the 
usual  devitalizing  period  and  free  entrance  is  made  to  the  pulp,  cutting 
away  all  insensitive  portions;  if  pulp  nodules  can  be  lifted  away  pain- 
lessly, they  are  removed,  and  a  fresh  application  of  arsenic  is  made, 
to  remain  again  several  days.  In  all  of  these  cases,  to  effectually 
de\italize  it  may  be  necessary  to  apply  a  paste  of  arsenic  trioxide  in 
glycerin,  or  in  one  of  the  essential  oils. 

Before  apphdng  the  arsenic  to  the  pulp  the  latter  is  always  to  have 
been  quieted  and  its  superficies  sterilized. 

During  the  application  all  pressure  is  to  be  avoided  or  inflammation 
will  be  induced,  w-hich  defeats  the  absorption  of  the  arsenic  and  causes 
needless  pain  as  well. 

'  Flagg  2  Ibid. 


ACCIDENTS  WITH  ARSEXIC  429 

If  the  pulp  be  much  diseased  at  the  point  of  exposure  it  is  better 
to  apply  the  arsenic  to  healthy  dentine  at  another  portion  of  the  cavity, 
or  in  a  pocket,  and  apply  analgesics  at  the  point  of  exposure. 

Symptoms.  A  vast  majority  of  pulps  die  with  no  more  pain  than 
the  slight  sensation  of  throbbing  or  fullness  due  to  the  gradual  and 
rapid  production  of  bulbar  stasis.  In  these  cases  the  absorption  of 
the  arsenic  has  been  prompt  and  the  irritative  effects  less  than  the 
paralyzant.  In  some  cases  the  throbbing  pain  may  be  felt  shortly 
after  application  and  may  pass  away  rapidly.  In  others  the  application 
must  be  removed  and  the  pulp  quieted  before  the  end  of  the  sitting. 
In  others  again  the  pain  may  begin  several  hours  after  application  and 
either  pass  promptly  into  the  sensation  of  hea^y  fulness  or  it  may 
become  paroxysmal.  If  endured  for  about  two  hours  this,  as  a  rule, 
gradually  or  suddenly  ceases.  If  applied  to  healthy  dentine  in  sound 
teeth  the  pain,  if  any,  will  be  delayed,  and  if  applied  to  sound  dentine 
of  teeth  which  have  pulps  elsewhere  exposed,  little  pain  is  produced 
if  the  pulp  be  kept  under  the  influence  of  an  analgesic. 

Not  infrequently  when  the  arsenic  is  applied  to  the  dentine,  whether 
for  twenty-four  hours  or  longer,  the  pain  and  suffusion  of  venous 
hypersemia  may  occur. 

In  cases  of  secondary  dentine  or  nodules  pain  may  supervene,  no 
matter  whether  the  arsenic  be  applied  to  the  dentine  or  the  pulp. 
The  amount  of  pain  produced  seems  to  depend  more  upon  the  con- 
dition of  the  pulp  than  upon  other  considerations.  Vigorous,  healthy, 
and  diseased  pulps  are  apt  to  respond  to  arsenic.  It  is  assumed  that 
absorption  is  incomplete. 

Accidents  with  Arsenic.  If  a  portion  of  an  arsenical  apphcation 
escape  from  beneath  its  covering,  it  may  destroy  much  or  a  little  gum 
tissue,  according  to  the  amount  which  escapes. 

The  arsenic  may  attack  the  gum  festoon,  inducing  in  it  stasis 
followed  by  necrosis.  The  gum  assumes  a  purplish  turgidity,  which 
later  changes  to  a  dirty-yellow  slough. 

The  bone  is  usually  devitalized  for  a  distance. 

If  the  necrosis  be  self-limited,  as  is  usually  the  case,  a  small  seques- 
trum comes  away  after  a  few  weeks. 

In  some  cases  the  arsenic  may  follow  the  festoon  of  the  gum  of  one 
or  more  teeth,  causing  disagreeable  sloughs  and  ulcerations.  It  may 
follow  the  pericemental  tract,  kill  the  pericementum,  and  the  tooth 
drops  out.  The  alveolar  process  about  one  or  several  teeth  may  be 
devitalized  and  a  sequestrum  occur  which  includes  the  teeth.    Certain 


430     REMOVAL  OF  DEXTAL  PULP  AND  ROOT-CANAL  FILLING. 

toothache  nostrums  are  sold  which  contain  arsenic.  Dr.  G.  C.  Chance^ 
records  a  case  of  arsenical  necrosis  occurring  from  this  source.  Dr. 
J.  E.  Powers^  records  a  case  in  which  extensive  necrosis  occurred  from 
the  use  of  colored  woollen  yarn  (as  a  cleanser  of  interdental  spaces) 
which  contained  arsenic  used  in  the  dye. 

From  the  infirmary  of  the  Philadelphia  Dental  College  was  referred 
to  the  oral  clinic  a  case  of  extensive  coagulation  necrosis,  resulting 
from  the  rubbing  of  "toothache  drops"  upon  the  gum.  Analysis 
showed  the  preparation  used  to  contain  arsenic.  Collapse  from  blood 
poisoning  being  the  immediate  danger,  the  child  was  operated  upon 


Boenning's  case  of  coagulation  necrosis  due  to  arsenic;  shows  exposed  and  blackened  alveolar 

process.    . 

by  Prof.  Boenning  for  drainage  of  the  parts.  During  the  recovery, 
the  teeth  from  the  right  lower  cuspid  to  the  left  lower  second  temporary 
molar,  and  the  gums  over  the  process,  were  lost,  leaving  a  blackened 
alveolar  process  to  be  later  removed  surgically  (Fig.  390). 

Arsenic  is  liable  to  pass  through  the  apical  foramina  of  unformed 
or  much  resorbed  roots.  It  may  possibly  pass  through  mature  roots, 
when  an  application  is  placed  high  up  in  the  canal,  rarely  when  applied 
under  normal  conditions  (as  recorded  by  some),  or,  as  occurred  in  one 
case,  by  the  application  being  pushed  through  the  apex.  It  may  be 
forced  through  in  the  act  of  broaching,  or  through  the  subsequent  use 
of  the  cataphoric  current  or  pressure  anaesthesia  without  the  prelimi- 
nary precaution  of  removing  the  arsenic. 


1  Proceedings  of  the  Academy  of  Stomatology,  Philadelphia,  1898. 

2  International  Dental  Journal,  November,  1902. 


ACCIDENTS  WITH  ARSENIC.  43 1 

Dr.  J.  C.  Curry^  exliibited  to  me  a  case  of  an  upper  central  incisor 
which  loosened  about  three  days  after  pulp  extraction  and  canal  filling. 
The  pulp  was  apparently  vital  at  the  apical  end  when  extirpated. 
The  crown  and  cervical  half  of  the  root  were  suffused,  the  apical  half 
was  normal  in  color,  but  the  foramen  was  rather  large.  The  gum 
showed  no  sign  of  sloughing,  but  the  root  was  entirely  denuded  of 
pericementum.  There  was  no  hemorrhage  or  appearance  of  pus  in 
the  alveolus  when  the  tooth  was  extracted  with  the  fingers.  In  most 
of  the  extensive  cases  of  arsenical  necrosis,  the  paste  made  of  finely 
ground  arsenic  and  creosote  has  been  used. 

In  some  cases  arsenic  has  been  applied  to  perforations  made  through 
the  sides  of  roots  under  the  impression  that  the  vital  tissue  found  was 
pulp  tissue.  In  such  case  its  necrotic  effects  will  be  noted  upon  the 
gum  overlying  the  root  apex  or  over  the  perforation,  the  tooth  being 
loosened  and  extruded  and  may  possibly  be  lost. 

E.  C.  Kirk-  has  recorded  several  cases  of  loss  of  teeth  from  arsenical 
necrosis  of  the  pericemental  tissue  following  the  use  of  mummifying 
paste  to  pulp  stumps  previously  impregnated  with  arsenic.  His  theory 
is  that  the  arsenic  was  liberated  by  the  aflSnity  of  the  ingredients  of 
the  mummifying  paste  for  the  proteid  constituents  of  the  pulp  tissue. 

Such  dangers  as  these  demand  that  extreme  precautions  be  taken 
against  the  careless  use  of  quantities  of  the  agent.  The  rules  laid 
down  should  be  adhered  to. 

The  only  cure  of  the  condition  consists  in  the  thorough  removal  of 
every  particle  of  the  arsenic.  Any  projecting  masses  of  oedematous 
gum  should  be  cut  away,  as  they  are  dead  and  will  slough  at  any  rate, 
and  a  freer  access  to  deep  parts  is  had — the  blood-flow  may  itself  wash 
away  the  arsenic.  The  forcible  washing  should  be  prolonged  and 
repeated,  Dialyzed  iron  or  tincture  of  iodine  should  be  applied  with 
a  view  to  possible  neutralization  of  the  arsenic. 

The  editor,  in  a  case  of  known  application  of  arsenic  to  an  obscure 
perforation,  succeeded  in  causing  regeneration  of  tissue  by  removing 
surgically  the  dead  tissue  and  inviting  regeneration. 

It  may,  therefore,  be  that  after  minute  portions  of  arsenic,  forced 
through  foramina,  exert  their  full  effect,  the  resulting  dead  tissue  may 
be  removed  by  resorption  or  even  exfoliation;  indeed,  this  result  has 
been  noted  in  which  no  other  explanation  seemed  possible. 

If  the  teeth  are  loosened  and  lost  as  the  result  of  arsenical  necrosis, 

1  Private  communication,  July  14,  1904  ;  too  late  to  make  tests,  which  may  be  reported  later. 

2  Dental  Cosmos,  October,  1903. 


432      REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING. 

either  beginning  at  the  gum  margin  or  at  the  apical  space,  the  alveolus 
will  exhibit  a  bare  periphery  and  even  some  odor  of  putrefaction  may 
be  present.  The  alveolus  should  be  sterilized  and  the  walls  burred 
away  to  a  tissue  capable  of  healthy  granulation. 

If  suffusion  occur,  essential  oils  or  phenol  should  be  avoided  in  the 
subsequent  treatment,  as  they  tend  to  set  the  color  by  acting  as  a 
mordant  (Kirk),  rendering  bleaching  difficult.  After  the  pulp  is 
removed  it  is  well  to  at  once  bleach  by  the  use  of  25  per  cent,  ethereal 
pyrozone,  after  which  the  canal  may  be  filled. 

REMOVAL  OF  THE  PULP. 

At  the  end  of  four  or  five  days  the  dressing  seals,  and  cotton  con- 
taining the  paste  are  removed,  the  cavity  freely  syringed  with  hydrogen 
dioxide,  and  the  rubber-dam  applied.  Large,  sterilized  rose  burs  are 
used  to  open  the  pulp  chamber  freely  and  to  remove  all  softened 
dentine. 

The  cavity  is  now  to  be  given  such  form  that  pulp  broaches  may  be 
passed  directly  and  freely  to  the  apex  of  each  root.  This  rule  is  to  be 
followed,  no  matter  how  much  tooth  substance  is  sacrificed  to  carry  it 
into  effect.  As  the  future  health  of  the  tooth  depends  almost  entirely 
upon  the  thoroughness  with  which  each  canal  is  cleansed,  sterilized, 
and  hermetically  sealed  at  the  apex,  it  is  evident  that  the  removal  of 
crown  tissue  is  a  small  evil  compared  with  incomplete  entrance  to  and 
cleansing  of  a  canal. 

A  new  and  perfect  pulp  broach  is  dipped  in  carbolic  acid  and  gently 
passed  to  the  apex  of  the  root;  the  teeth  of  the  broach  are  turned  away 
from  the  pulp  until  the  instrument  is  fully  inserted,  when  the  broach 
is  turned  so  that  its  teeth  shall  engage  the  entire  length  of  the  pulp, 
which  may  then  usually  be  removed  entire.  The  finest  Donaldson 
cleanser  may  sometimes  be  used  in  this  manner.  Cotton  may  be 
wound  on  a  fine  Swiss  broach  and  twisted  into  the  pulp  to  engage  it. 

In  multirooted  teeth  the  largest  canal  may  have  its  pulp  removed 
as  above  indicated.  As  a  rule,  the  smaller  canals  require  enlarge- 
ment. 

Gates-Glidden  drills  are  passed  into  the  mouths  of  canals,  slightly 
enlarging  them.  Kerr  or  Downie  broaches — a  form  of  tapering  twist 
drill— are  then  passed  into  the  canals  as  far  as  they  will  go  and  turned, 
reaming  the  canal.  As  they  are  of  fine  temper  and  conform  to  the 
curve  of  the  canal,  they  are  comparatively  safe.    The  small  sizes  are 


REMOVAL  OF  THE  PULP. 


433 


used  first,  then  the  larger  ones.  They  may  be  had  for  the  straight  and 
angle  hand-pieces.  Successive  sizes  of  nicely  tempered  S"v\'iss  broaches 
may  be  used  as  canal  reamers  until  larger  instruments  can  be  used. 
Of  these  the  writer  prefers  the  Downie  reamers  (Fig.  392). 

Gates-Glidden  drills  may  again  be  used  or  Donaldson  cleansers 
may  be  employed  to  rasp  the  sides  of  the  canal  not  touched  by 
the  Downie  or  Swiss  broaches. 

In  place  of  drills  the  process  of  canal  enlargement  devised  by 
Callahan^  may  be  employed.  The  general  cavity  wall  is  varnished  to 
prevent  the  action  of  the  acid  upon  the  dentine,  and  by  means  of  a 
pair  of  Flagg's  dressing  pliers  or  a  minim  dropper  a  drop  of  sulphuric 


Fig.  391. 


Fig.  392. 


Kerr  root-canal  reamers  and  broaches. 


Downie  root-canal  reamers  and  broaches. 


acid  (50  per  cent,  solution)  is  deposited  at  the  mouth  of  the  canal 
to  be  operated  upon.  The  finest  size  of  Donaldson's  canal  cleanser 
is  then  passed  into  the  canal  as  far  as  it  will  go,  using  a  pumping 
movement  to  carry  the  acid  farther  into  the  canal  and  to  scrape  the 
canal  walls  softened  by  the  action  of  the  acid.  The  acid  chemically 
destroys  any  organic  matter — i.  e.,  pulp  tissue — present,  releases  the 
calcium  of  the  dentine  from  its  combination,  and  forms  calcium 
sulphate,  which  is  mechanically  removed  by  scrapers.  The  operation 
is  continued  until  the  apex  of  the  root  is  reached.  F.  T.  Hayes  suggests 
the  use  of  aqua  regia  as  less  injurious  to  broaches ;  lactic  acid  is  also 
less  injurious.     When  the  cleanser  will  not  enter  readily  it  is  well  to 


1  Proceedings  of  the  Ohio  State  Dental  Society,  1894. 
28 


434     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING. 


file  away  the  barbs  from  an  old  cleanser  and  leave  it  roughened, 
and  to  use  it  for  a  time  with  the  acid  until  the  cleanser  proper  can  be 
employed.  Iridioplatinum  or  gold  broaches  may  be  used  for  this 
purpose. 

In  the  canals  of  posterior  teeth  short  cleansers  are  mounted  in  a 
chuck  handle  and  the  shank  sharply  bent  at  a  right  or  obtuse  angle. 


Fig.  393. 


Fig.  395. 


Fig.  396. 


Dr.  Donaldson's  pulp-canal  cleansers. 

If  the  cleanser  bind  in  the  canal  it  should  be  grasped  with  the 
thumb  and  forefinger  and  given  a  straight  pull  to  relieve  it. 

The  use  of  5  per  cent,  formalin,  tannin,  or  alum,  to  be 
specially  applied  about  three  days  after  the  application  of 
arsenic,  has  been  suggested  for  the  toughening  of  pulps.  Their 
use  necessitates  a  visit  for  their  special  application.  They 
toughen  the  pulp,  but  this  is  of  little  advantage  in  the  finer 
canals  and  not  needed  in  the  larger  ones. 

The  point  of  importance  is  the  removal  from  the  pulp  canal 
of  all  removable  portions  of  pulp  tissue,  and  an  enlargement 
sufficient  to  admit  a  satisfactory  root  filling.  It  is  an  open 
question  whether  in  multirooted  teeth  this  is  ever  complete,  or 
whether  it  is  necessary  that  it  be  made  absolutely  so,  regardless  of 
other  dangers. 

A  perfectly  safe  rule  for  mechanical  procedures  is  as  follows:  Use 
drills  only  when  they  advance  readily  into  the  root  lumen;  prefer 
Downie  broaches  and  Donaldson  cleansers  under  other  circumstances. 
Advance  no  large  reamers  into  delicate  apical  portions  of  roots,  as  a 
lateral  perforation  may  be  made.  If  a  fine  broach  cannot  be  passed 
through  the  apical  foramen,  do  not  attempt  its  enlargement. 


ROOT-CANAL  FILLING.  435 

If  doubt  exist  as  to  the  presence  of  a  portion  of  pulp  in  the  apex 
of  the  root,  papain  paste  may  be  placed  in  the  canals  for  a  few  days 
to  digest  the  remaining  pulp  tissue.     (See  Pulp  Digestion.) 

If  the  pulp  be  removed  to  the  end  of  the  root  and  the  canal  sealed 
to  that  point  with  a  mechanically  perfect  and  antiseptic  root  filling, 
it  is  improbable  that  any  future  trouble  will  arise;  and  it  is  better  that 
any  such  trouble  should  be  subsequently  treated  than  that  immediate 
trouble  should  be  set  up  by  perforation. 

It  has  been  recommended  that  all  canals  should  be  drilled  or  scraped 
to  remove  the  organic  matter  attached  to  the  periphery  of  the  dentine 
The  Callahan  method  accomplishes  this.  Such  organic  matter  may 
later  undergo  putrefaction  and  is  well  removed. 

If  the  operations  have  been  done  under  antiseptic  precautions  the 
root  is  ready  for  filling,  unless  irritation  of  the  apical  tissues  be  severe, 
in  which  case  a  sedative  antiseptic — e.  g.,  menthol  in  chloroform — on 
cotton  should  be  sealed  in  the  canal.  The  gum  should  be  painted  with, 
iodine  as  a  counterirritant  and  the  subsidence  of  the  symptoms  awaited^ 
(See  Aseptic  Apical  Pericementitis.) 

THE  ROOT-CANAL  FILLING. 

The  features  to  be  possessed  by  a  canal  filling  should  be:  first,  it 
should  be  non-irritating;  second,  it  should  hermetically  seal  the  canal; 
third,  it  should  be  unalterable  in  the  conditions  surrounding  it.  If 
possible,  it  should  be  continuously  antiseptic,  and  be  removable  if 
subsequent  conditions  ever  demand  its  removal. 

These  conditions  may  all  be  fulfilled  in  the  well-opened  roots  by 
the  use  of  temporary  stopping,  gutta-percha  or  wax,  each  made  anti- 
septic by  combining  with  it  suitable  ingredients.  Each  may  be  gently 
melted  in  a  spoon  held  over  a  flame  and  a  third  of  its  bulk  of  aristol 
or  iodoform  incorporated  with  it.  When  partly  cold  it  is  moulded 
into  cones  suitable  for  introduction  into  the  canal.  This  may  be  done 
on  a  glass  slab  by  rolling  with  an  ivory  paper-cutter  or  spatula.  When 
the  canal  is  prepared  and  its  walls  thoroughly  dried  by  means  of  hot 
air,  a  trifle  of  eucalyptol  is  introduced  into  the  canal  and  all  excess 
removed,  or  a  little  chloro-percha  is  introduced.  The  pointed  section 
of  a  cone  of  temporary  stopping  or  gutta-percha  is  attached  by  heat 
to  a  canal  plugger  and  carried  to  the  apex  of  the  canal,  where  it  is 
firmly  yet  gently  compressed.  Other  sections  are  added  until  the 
canal  is  one-half  or  three-fourths  filled.    Over  this  is  placed  oxychloride 


436     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING. 

of  zinc  or  zinc  phosphate  made  antiseptic  by  the  addition  of  aristol 
while  mixing.  Whether  the  crown  filHng  shall  be  introduced  at  the 
same  sitting  or  not  depends  upon  the  general  irritability  of  the  tissues 
of  the  patient  and  the  operator's  convenience.  As  a  rule,  it  is  well 
to  temporarily  fill  the  crown  cavity  with  base-plate  gutta-percha^ 
(Fig.  397),  apply  a  good  counterirritant  to  the  gum  over  the  apex,  and 
permit  the  apical  tissues  to  recover  their  normal  tone.  In  a  vast 
majority  of  cases  this  immediate  root  filling  is  accompanied  by  a  suc- 
cessful issue,  whether  some  apical  irritation  arise  or  not,  and  as  a  rule 
it  does  not. 

In  case  of  an  open  foramen  a  long  cone  is  rolled;  this  is  tried  in  the 
canal  and,  passing  through  the  foramen,  will  irritate  the  tissue.  It  is 
cut  ofiF  a  line  at  a  time  until  it  stops  at  the  foramen  without  irritation. 
To  allow  for  slipping  of  the  cone  a  half-line  more  is  removed.    The 


Fig.  397. 


Fig.  398. 


Hoot-canal  filling:  A,  gutta-percha; 
B,  oxychloride  of  zinc. 


A,  perforation  through  side  of  apex;  D,  cone  of 
gutta-percha  passing  through ;  B,  portion  to  be 
cut  off  ;  C,  portion  of  canal  not  treated. 


apex  of  the  canal  is  moistened  with  thick  antiseptic  chloro-percha  and 
a  quarter-inch  of  cone  packed  into  the  root  canal,  which  it  should 
exactly  fit  (Fig.  398).  A  bit  of  sterilized  grafting  sponge  may  be 
inserted  beyond  the  apex  and  the  canal  then  filled. 

In  the  case  of  wax,  yellow  beeswax  and  aristol  or  wax  and  paraform 
are  to  be  preferred  to  paraffin.  The  cone  is  thrust  into  a  dry  canal, 
packed  cold  for  a  distance,  and  then  the  point  of  a  warmed  Evans 
root  drier  is  used  to  melt  and  pump  it  into  the  canal  until  the  latter 
is  partly  filled,  when  oxychloride  of  zinc  or  antiseptic  zinc  phosphate 
is  used  to  cover  it. 

In  open  canals  thin  oxychloride  of  zinc  may  be  introduced.  It  is 
carried  to  place  upon  shreds  of  cotton.  Some  operators  prefer  to 
place  a  shred  of  cotton  saturated  with  an  antiseptic  oil  in  the  apex 
of  the  root  canal.     It  has  been  claimed  that  the  cotton  is  converted 


1  White  base-plate  gutta-percha  may  now  be  had. 


ROOT-CANAL  FILLING.  437 

into  amyloid.  I  have  conducted  experiments  to  determine  this  point, 
and  found  that  it  can  hardly  be  true  for  oxychloride  of  zinc,  though 
true  when  cotton  is  placed  in  a  chloride  of  zinc  solution. 

Good  results  are  nevertheless  obtained  by  the  method,  owing  to  the 
antiseptic  property  of  the  oxychloride  of  zinc.  It  is  very  difficult  of 
removal  and  should,  therefore,  only  be  employed  after  temporarily 
dressing  the  canal  with  a  sedative  antiseptic,  unless  it  be  desired  to 
take  the  risk  of  apical  pericementitis  which,  in  these  cases,  is  a  rare 
sequel. 

Antiseptic  chloro-percha — a  solution  of  gutta-percha  in  chloroform 
with  aristol  or  iodoform  added — may  be  used  on  a  twist  of  cotton  as  a 
filling  in  place  of  a  cone.  It  is  more  difficult  of  removal  than  the 
cone,  owing  to  the  presence  of  the  cotton  fibres.  Ottolengui  recom- 
mends that  a  number  of  pieces  of  floss  silk  about  an  inch  long  be 
saturated  with  chloro-percha  and  dried.  These  are  to  be  introduced 
into  the  previously  placed  chloro-percha  and  the  end  allowed  to  remain 
in  the  pulp  chamber.  If  removal  be  necessary  the  floss  may  be  engaged 
and  removed.  If  a  root  can  be  drilled  for  a  free  opening  the  gutta- 
percha cone  can  largely  be  removed  with  the  drill. 

In  the  finer  canals  an  antiseptic  eucalyptol  solution  of  gutta-percha 
is  preferable  to  chloro-percha.  Dr.  J.  C.  Blair  has  introduced,  under 
the  name  of  "  Forma-Percha,"  such  a  solution  containing  oil  of  cassia 
and  paraform.  Its  uses  as  a  root  filling  are  identical  with  those 
of  chloro-percha.  Its  removability  lies  in  its  weakness  of  cohesion 
after  drying.  For  use  it  should  be  warmed  into  a  creamy  mass  and 
used  with  cotton.  Cotton  saturated  with  wood  creosote  has  been 
used  for  the  finer  canals,  but  cotton  is  an  absorbent  and  after  losing 
the  creosote  may  take  up  deleterious  matter  unless  mechanically  anti- 
septic coverings  are  placed  over  it.  If  used  it  should  be  confined  to 
the  apical  third  of  doubtful  roots.  With  oxychloride  of  zinc,  chloro- 
percha,  or  other  impervious  materials  in  its  meshes  cotton  is  probably 
a  root  filling  of  more  permanency.^ 

1  When  cotton  is  used  as  a  root  filling  or  a  vehicle  for  non-absorbent  substances  it  should 
be  mounted  on  a  delicate  Swiss  broach.  The  latter  should  have  its  hard  temper  drawn 
by  annealing  in  a  test-tube  over  a  flame.  The  heat  is  applied  at  the  shank,  and  the  tube 
is  to  be  moved  over  the  flame  so  that  a  pigeon-blue  color  runs  out  to  the  tip  of  the  blade. 
Such  broaches  are  fit  for  reamers,  and  are  of  splendid  temper.  The  tip  should  be  removed 
with  scissors,  so  that  penetration  of  the  cotton  may  be  avoided.  The  wisp  of  cotton  is  to 
be  laid  upon  the  left  forefinger,  the  broach  laid  upon  it,  the  thumb  closed  down,  and  the 
broach  twisted  with  the  right  thumb  and  forefinger,  the  left  ones  being  then  used  to  stroke  the 
cone  to  symmetrical  form.  This  requires  some  practice.  As  a  swab  this  is  always  twisted  to 
the  right.  As  a  dressing  it  is  passed  into  the  root,  twisting  to  the  right.  When  placed  the 
broach  is  given  frn-o  turns  to  the  left,  is  slightly  withdrawn  and  then  pressed  in  again.  This 
causes  the  cotton  to  be  crimped  upon  itself.  Raw  cotton  is  preferable  to  absorbent  M'hen  used 
for  other  purposes  than  as  a  root  swab. 


438     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING. 

The  secret  of  success  in  root-canal  filling  lies  perhaps  more  with  the 
prevention  of  infection  from  the  mouth  than  with  the  character  of 
the  material  placed  in  the  apex  of  the  root  canal.  Nevertheless,  the 
prevention  of  ingress  of  fluids  from  the  apical  tissues  seems  to  be 
necessary;  at  least,  the  entrance  of  such  fluids  invites  earlier  infec- 
tion. 

M.  L.  Rhein  has  recorded  an  opinion  that  recurrent  sepsis  may 
often  arise  by  way  of  the  circulation.  The  possibility  of  this  is  not 
to  be  denied,  but  my  experience  leads  me  to  doubt  its  frequency  as 
a  cause.     Opportunity  for  oral  infection  is  usually  sufficient. 

Accidents  Occurring  during  Canal  Opening.  During  the  mechan- 
ical enlargement  of  canals  or  during  pulp  removal  portions  of  broaches 
or  drills  may  be  broken  off  in  the  canal.  Their  removal  is  at  times 
difficult  or  practically  impossible.  If  lying  loosely  in  the  canal  a  probe 
magnetized  by  rubbing  upon  a  steel  magnet  or  by  contact  with  the 
field  magnet  of  a  dynamo  will  remove  it.  Flagg  recommended  a  power 
magnet  attached  to  a  probe.  The  magnet  is  to  be  energized  by  an 
electric  current. 

Wrapping  a  Swiss  broach  with  cotton,  the  fibres  may  at  times  be  made 
to  engage  the  barbs  of  a  loose  broach. 

A  Donaldson  cleanser  will  also  at  times  engage  the  barbs  of  the 
broken  instrument. 

The  removing  instrument  is  passed  to  one  side  of  the  instrument  to 
be  removed  and  pressed  against  it  as  withdrawn.  The  instrument  is 
thus  gradually  jigged  out. 

Moving  the  broach  or  drill  back  and  forth  while  sulphuric  acid  or 
sodium  dioxide  solution  is  about  it  will  sometimes  loosen  it. 

If  very  deeply  placed  common  salt  may  be  packed  over  the  broach, 
moistened,  and  sealed  in  in  the  hope  of  rusting  it.  Tincture  of  iodine 
will  rapidly  disintegrate  steel  placed  in  it,  but  repeated  applications 
are  necessary  to  produce  the  same  effect  in  a  canal. 

Sulphuric  or  nitric  acid  or  aqua  regia  or  25  per  cent,  pyrozone  may 
be  sealed  in  to  effect  its  chemical  solution.  The  tip  of  a  fine  Donaldson 
cleanser  deeply  seated  in  the  apical  third  of  a  fine  canal  is  practically 
irremovable.  If  the  root  has  given  no  previous  trouble,  strong 
and  persistent  antiseptics,  such  as  iodoform,  are  to  be  placed  over 
it  and  the  attempt  to  remove  considered  unwarrantable.  The  head 
of  a  Gates-Glidden  drill  is  to  be  saturated  with  sodium  dioxide 
or  sulphuric  acid  and  the  attempt  is  made  to  jig  the  piece  loose;  failing 
this  an  attempt  is  to  be  made  to  pass  through  the  opening  between 


ACCIDENTS  IN  CANAL  OPENING. 


439 


the  blades  so  that  permanently  antiseptic  materials  may  be  made  to 
go  beyond  the  drill,  in  which  case  its  presence  is  harmless. 

Dr.  W.  S.  How  has  introduced  the  split  and  threaded  cone  socket 
shown  in  Fig.  400,  which  may  be  useful  at  times. 


Fig.  399. 


Fig.  400. 


Improved  Gates-Glidden  nerve-canal  drill  for  engine  work. 

In  use  the  canal  is  enlarged  after  a  direct  open- 
ing has  been  made  to  it  and  the  cone  is  intro- 
duced and  rotated. 

In  all  cases  the  forcing  of  bits  of  broaches  into 
the  apical  tissues  during  efforts  at  removal  is  to 
be  carefully  avoided.  If  it  occur,  however,  it 
will  produce  a  chronic  apical  pericementitis  if 
not  excite  a  septic  condition.  The  cure  lies  in 
amputation  of  the  root  apex,  though  at  times 
levelling  the  broach  with  the  root  end  through 
an  external  opening  has  been  successful. 

Perforations.  A  drill  passed  through  the  apical 
foramen  enlarges  it  unduly.  The  condition  simu- 
lates an  imperfectly  completed  foramen  and  is 
treated  as  for  that  condition.     (See  p.  436.) 

A  Gates-Glidden  drill  may  perforate  a  root  near 
the  apex  by  passing  through  the  wall  of  the  canal 
in  a  direct  line  with  the  canal,  while  the  root  end 
may  be  curved  (Fig.  398). 

A  finely  pointed  root  may  be  perforated  later-  strument  for  engaging  the 

„       -  ,  „  -        "^  \    ...  shank  of  a  Gates-Glidden 

ally  by  the  use  oi   too  large  a  drill  or  reamer,  driii. 

The  part  should   be  thoroughly  sterilized  and 

the  hemorrhage  checked  by  the  use  of  adrenalin  chloride  1  :  1000  plus 

chloretone,^  and  a  carefully  prepared   gutta-percha  point  is   to   be 

adapted  to  the  opening.    If  subsequent  trouble  arise  amputation  or 

extraction,  perfect  root  filling,  and  replantation  may  be  resorted  to. 


Split  and  threaded   in- 


1  Prepared  by  Parke,  Davis  &  Go. 


440     REMOVAL  OF  DENTAL  PULP  AXD  ROOT-CAXAL  FILLING. 

If  the  perforation  be  readily  reached  the  inner  walls  should  be  bevelled 
and  a  smooth  plaque  of  low-heat  white  gutta-percha  should  be 
adapted,  its  edges  sealed,  and  zinc  phosphate  or  oxychloride  of  zinc 
packed  over  it  to  secure  it  in  place.  Soft  copper  amalgam  gently 
tapped  to  place  and  later  hardened  by  the  wafering  process  is  valu- 
able. In  such  cases  the  canal  apex  is  filled  as  usual.  With  a  diffi- 
cult lateral  perforation  a  bit  of  sterilized  grafting  sponge  may  be 
placed  in  the  tissue  beyond  the  perforation,  and  against  this  the  gutta- 
percha or  copper  amalgam  may  be  packed.^ 

Partial  Removal  of  Pulp.  The  Cobalt  method  of  pulp  treatment 
has  been  alluded  to.  Wm.  Herbst,  of  Bremen,  advanced  the  idea  that 
if  the  bulbous  portion  of  the  pulp  be  devitalized  by  cobalt  and  removed, 

Fig.  401.  Fig.  402. 


Lateral  perforation  due  to  holding  a  bar  at  a  Herbst's  method  of  preser-vdng  pulp 

wrong  angle  to  the  axis  of  the  root:  A,  root  canal  stumps, 

subsequently  filled  with  gutta-percha;  B,  perfo- 
ration filled  ^"ith  a  fitted  cone  of  gutta-percha; 
C,  oxychloride  of  zinc. 

leaving  the  root  portions,  the  latter  will  remain  vital,  if  protected  after 
a  manner  described  by  him.  The  bulbous  portion  of  the  pulp  is  cut 
away  and  the  pulp  chamber  enlarged  by  means  of  large  rose  burs. 
Over  the  pulp  stumps  a  cylinder  of  tin-foil  is  laid,  and  burnished  to 
fit  the  floor  of  the  pulp  chamber,  without  pressure  upon  the  pulp 
stumps  (Fig.  402).  Over  this  a  filling  is  placed.  Herbst  claims 
that  the  pulp  stumps  will  remain  vital.  Were  this  to  be  depended 
upon,  it  would  be  a  marked  sa^dng  of  time  and  trouble,  and  would 
lessen  the  chances  of  pericementitis  subsequent  to  pulp  removal;  but 
when  it  is  known  that  the  cobalt  of  Herbst  is  metallic  arsenic,  the 
ultimate  death  and  decomposition  of  the  pulp  remnants  segm  almost 
inevitable,  and  in  fact  does  occur.  The  method  should  not  be  em- 
ployed. 

1  G.  Brunton,  Eng.,  Dental  Cosmos,  1900. 


MUMMIFICATION  OF  THE  PULP.  44I 

MXJMMIFICATION  OF  THE  PULP. 

Many  experiments  have  been  performed  relative  to  lea\dng  m  situ 
portions  of  pulps  and  covering  them  ^^th  substances  having  for  their 
object  the  chemical  alteration  of  the  pulp  tissue,  so  that  no  peri- 
cementitis shall  result  from  its  putrefaction.  The  first  effort  in  this 
direction  is  credited  to  Witzel  (1874). 

W.  D,  Miller/  after  many  experiments  with  various  materials,  has 
shown  that  none  but  the  most  powerful  and  penetrating  antiseptics 
have  value  as  permanent  sterilizers.  These  are  the  cyanide,  bichloride, 
and  salicylate  of  mercury,  sulphate  of  copper,  and  oil  of  cinnamon. 
Orthocresol,  carbolic  acid,  trichlorphenol,  and  zinc  chloride  penetrate 
the  pulp  tissue  rapidly,  but  are  too  diffusible,  their  effects  disappearing 
in  a  few  weeks. 

He  classifies  salicylic  acid,  eugenol,  camphophenique,  hydro- 
naphthol,  a-naphthol  and  /^-naphthol,  aceticotartrate  of  aluminum, 
and  some  essential  oils,  resorcin,  thallin,  sulphocarbolate  of  zinc,  etc., 
as  being  of  doubtful  value. 

Those  nearly  or  quite  worthless  are  iodoform,  basic  anilin  coloring 
matters,  borax,  boric  acid,  dermatol,  europhen,  calcium  chloride, 
hydrogen  dioxide,  sozoiodol  salts,  tincture  of  iodine,  spirit  of  camphor, 
and  naphthalin. 

The  preparation  giving  the  best  results  consisted  of  mercuric  chloride, 
0.0075  gram;  thjTiiol,  0.0075  gram,  in  tablet  form. 

The  pulp  is  devitalized;  the  crown  portion  and  all  the  root  portion 
readily  accessible  are  removed ;  one  of  the  tablets  is  placed  in  the  pulp 
chamber,  crushed  by  means  of  an  amalgam  plugger,  and  covered  with 
gold-foil.  The  mercury  salt  tends  to  discolor  the  crown  of  the  tooth, 
so  that  its  employment  should  be  restricted  to  the  posterior  teeth; 
indeed,  the  necessity  for  its  use  would  be,  as  a  rule,  found  with  these 
teeth,  being  those  from  which  it  is  most  difficult  to  extract  pulp 
remnants.  IMiller  expresses  faith  in  the  power  of  oil  of  cinnamon  to 
permanently  sterilize  pulp  fragments. 

Theodore  Soderberg^  recommended  a  paste  composed  as  follows: 

9^ — Alum  exsic,  " 

Thymol, 

Glycerol.,  net    Sj. 

Zinci  oxid.,  q.  s.  to  make  a  stiff  paste. — ^I. 

It  is  preferable  to  add  the  zinc  oxide  as  needed  or  to  make  a  small 
quantity  of  the  paste  frequently,  as  it  gradually  hardens.    To  the  paste 

1  Proceedings  of  Columbian  Dental  Congress,  1893.  -  Dental  Cosmos,  November,  1895. 


442     REMOVAL  OF  DENTAL  PULP  AXD  ROOT-CAXAL  FILLING. 

used  a  crystal  of  cocaine  is  added  to  prevent  pain.  Bennette  (Eng.)  has 
advised  the  use  of  paraform  incorporated  in  the  paste,  for  its  well- 
known  antiseptic  and  hardening  effects.  Greenbaum  suggested  the 
use  of  a  drop  of  40  per  cent,  formaldehyde  solution  to  be  incorporated 
with  the  paste. 

Soderberg  reopened  cases  months  after  application  of  the  paste  to 
pulp  stumps,  and  found  them  shrunken  and  with  an  odor  of  thymol 
about  them. 

Fig.  403.  FiCx.  404. 


a,  caries  exposing  a  liorn  of  the  pulp.  a,  root  portion  of  pulp;  6,  mummifying  paste; 

c,  zinc  phosphate ;  d,  gold  or  amalgam. 

He  applied  the  paste  in  the  manner  shown  in  Figs.  403  and  404. 
In  1900,  Soderberg^  reported  the  use  of  the  paste  in  about  nine  hundred 
cases,"  of  which  two  hundred  and  twenty  were  test  cases  of  from  two 
to  six  years'  standing  He  claims  that  in  no  case  did  apical  pericemental 
disturbance  arise  from  the  use  of  the  paste  as  described. 

This  method  has  met  with  much  opposition  from  prominent  oper- 
ators, who  prefer  the  thorough  cleansing  and  filling  of  the  canals. 
No  doubt  the  rational  method  of  procedure  is  to  cleanse  the  canals 
as  well  as  possible  and  to  use  the  paste  against  unremovable  pulp 
stumps. 

The  best  results  were  obtained  when  arsenic  was  applied  for  a 
limited  time  only  in  order  that  the  arsenic  should  not  penetrate  too 
deeply.  In  view  of  Kirk's  observations  (p.  431)  this  M^ould  seem 
wise. 

While  the  paste  may  effect  mummification  of  entire  canal  filaments 
of  pulp,  leakage  is  always  imminent  about  shrunken  pulps,  and  the 
only  safeguard  is  the  antiseptic  effect  of  the  paste.  This  is  much 
enhanced  if  the  bulk  of  putrefiable  material  be  replaced  with  the  anti- 
septic paste  used  as  a  root  filling.  Many  such  root  fillings  have  done 
good  service  for  many  years. 

1  Dental  Cosmos.  2  items  of  Interest,  1898. 


DIGESTION  OF  THE  PULP.  443 

A  certain  percentage  of  failures  would  be  no  argument  against  the 
employment  of  the  method  when  indicated,  as  no  method  is  infallible 
in  all  circumstances,  and  particularly  in  those  in  which  the  method 
is  indicated. 

DIGESTION  OF  THE  PULP. 

Harlan  has  recommended  the  digestion  of  inaccessible  pulp  remnants 
with  a  vegetable  ferment.  The  pulp  chamber  is  dried  and  then 
moistened  with  a  1 :  300  solution  of  hydrochloric  acid  and  packed  with 
a  paste  composed  as  follows: 

9; — Papain,  gr.  v. 

Price's  pure  glycerin,  W\\v. 

1/200  liydrochloric  acid,  ITlv. 

Over  this  is  placed  a  layer  of  blotting-paper  soaked  in  liquid  vaselin. 
The  cavity  is  sealed  with  oxyphosphate  of  zinc  or  oxysulphate  of  zinc. 

The  paste  should  be  freshly  made  in  the  above  proportions,  reduced 
to  suit  the  quantity  needed.  The  application  requires  a  few  days 
to  reduce  the  pulp  tissue  to  a  jelly-like  digested  mass,  which  can 
readily  be  washed  away.  It  is  recommended  that  the  papain  be  kept 
in  a  dark-glass  bottle.  It  is  harmless  to  living  tissue  which  is  not 
digested.  Alcohols,  tannin,  lead,  mercuric  chloride,  nitric  acid,  and 
salts  of  heavy  metals  are  incompatibles. 

Such  pulp  digestion  is  only  a  preliminary  to  root  filling. 


CHAPTER    XIX. 
GANGRENE  OF  THE  PULP. 

Definition.  By  gangrene  of  the  pulp  is  meant  its  death  through  an 
interference  with  its  nutrition.  It  may  be  partial,  as  when  an  abscess 
in  the  pulp  or  violent  irritation  causes  the  bulbar  portion  to  die,  the 
canal  portions  being  found  alive;  or  when  only  one  canal  portion  is 
dead,  the  others  being  alive.    Either  dry  or  moist  gangrene  may  occur. 

Causes.  It  is  probable  that  a  construction  of  apical  root  tissue 
(hypercementosis)  about  the  pulp  may  so  constrict  it  as  to  bring  about 
its  death.  Sudden  shocks,  such  as  occur  from  thread,  string,  or  cigar 
biting,  or  blows  or  rapid  movement  in  regulating  or  wedging  or  non- 
fixation  after  regulation,  may  cause  torsion  or  tension  of  the  blood- 
vessels entering  the  apex  of  the  pulp. 

These  influences  may  either  cause  pulp  hyperemia  or  strangulation 
of  the  apical  bloodvessels,  or  possibly  an  area  of  apical  thrombosis, 
cutting  off  the  nutritive  supply  to  the  pulp.  Septic  or  aseptic  inflam- 
mation of  the  pulp  may  cause  its  total  death.  Death  of  pulp  tissue 
due  to  arsenic  produces  results  in  nowise  differing  from  gangrene, 
provided  the  pulp  be  left  m  situ. 

DRY  GANGRENE  OF  THE  PULP. 

Definition.  By  dry  gangrene  of  the  dental  pulp  is  meant  its  death 
in  toto  and  its  subsequent  transformation  into  a  dry,  shrivelled  mass 
occupying  thg  pulp  chamber  and  canal. 

Causes  and  Pathology.  If  the  pulp  die  and  remain  under  conditions 
which  exclude  bacteria  from  contact  with  it,  the  water  of  the  pulp 
may  be  removed,  leaving  the  organ  as  a  tough,  shrivelled  mass 
(Fig.  405).  The  conditions  most  favorable  seem  to  be:  (1)  pulp 
death  from  some  aseptic  cause;  (2)  constriction  of  the  apical  foramen; 
(3)  the  presence  of  secondary  dentine  over  the  bulbar  portion  of  the 
pulp;  (4)  the  capping  of  the  pulp  with  zinc  oxychloride  or  formagen 
paste;  (5)  the  covering  of  pulp  stumps  with  a  paste  containing  a  tanni- 
fying  substance,  such  as  alum,  formaldehyde,  or  tannin. 

The  water  necessary  to  putrefaction  is  abstracted,  either  naturally 
or  chemically,  and  probably  bacteria  are  at  the  same  time  excluded 


DRY  GANGRENE  OF  THE  PULP.  445 

either  mechanically  or  because  the  chemical  substances  used  have 
penetrated  the  pulp  tissue,  acting  as  antiseptics. 

Symptoms.  The  tooth  has  a  nearly  normal  color,  but  under  reflected 
light  is  seen  to  have  lost  perfect  translucency.  There  is  no  response 
to  thermal  or  electric  tests  for  pulp  vitality.  The  dentine  is  insen- 
sitive to  cutting  instruments  and  the  cuttings  upon  the  bur  have  no 
odor.  There  is  no  odor  or  fluid  in  the  pulp  canal  when  this  is  entered, 
and  the  pulp  is  found  as  a  tough,  dry  mass  not  unlike  that  seen  in  a 
dry  extracted  tooth  which  contained  a  vital 

,  ,  .  „  '  rry^  FlG.  405. 

pulp  at  the  time  ot  extraction,  ihese  cases 
are  relatively  rare. 

Tests  for  Pulp  Vitality.  The  diagnosis  of 
pulp  vitality  or  death  being  in  practice 
almost  daily  required,  the  decisive  tests  are 
here  indicated. 

A  tooth  containing  a  vital  pulp  is  trans- 
lucent; that  containing  a  dead  one  always 

onaniip  to  transmittpd   hVht  Dry  gangrene  of  the  pulp:  PN, 

opaque  to  transmittea  iigni.  p^^p  ^^^^^.  j^p^  shrivelled  pulp. 

An  electric  mouth  lamp  with  a  mirror  so  (From  a  specimen  of  puip  ex- 

,  n  1         T    1  1         tracted  intact  in  this  condition.) 

arranged  as  to  reflect  the  light  upon   the 

lingual  surface  of  the  tooth  will  supply  the  means  for  this  test.  In 
its  absence  strong  sunlight  may  be  reflected  by  means  of  a  mouth 
mirror,  but  is  not  nearly  so  good  a  means  as  the  electric  light 
(Fig.  331). 

If  the  tooth  be  isolated  by  means  of  rubber-dam  and  first  cold  water 
be  thrown  or  later  ethyl  or  methyl  chloride  be  sprayed  upon  it  or  upon 
the  filling  contained  in  it,  absence  of  response  will  indicate  either  pulp 
death  or  the  formation  of  a  quantity  of  secondary  dentine.  In  the 
latter  case  the  test  must  be  renewed  as  the  excavation  proceeds. 

A  hot  burnisher  or  hot  gutta-percha  applied  to  a  filling  or  dentine,  or 
very  hot  water  thrown  upon  an  isolated  tooth  should  provoke  at  least 
a  delayed  response  from  a  vital  pulp. 

Woodward  has  shown  that  if  a  few  cells  of  a  cataphoric  apparatus 
are  in  action  and  the  positive  electrode  be  applied  to  the  dentine  or 
metal  filling  in  a  vital  tooth,  while  the  negative  pole  is  at  the  cheek 
or  wrist  of  the  patient,  a  distinct  sensation  should  be  felt;  while  in 
case  of  a  dead  pulp  there  will  be  no  response.  A  mild  faradic  cur- 
rent has  also  been  used  for  the  test.  There  may  be  no  response 
through  a  metal  filling,  while  such  response  may  be  obtained  by 
packing  wet  cotton  against  the  dentine  after  some  drilling.     The  pos- 


446  GANGRENE  OF  THE  PULP. 

sibility  of  contact  of  the  filling  with  another  in  a  vital  tooth  is  to  be 
remembered.     Insulation  with  rubber-dam  is  indicated. 

In  doubtful  cases,  such  as  that  shown  in  Fig.  406,  the  ;r-ray  skia- 
graph is  valuable,  and  indicates  at  least  the  removal  of  the  filling  for 
further  diagnosis  and  treatment. 

A  strong  odor  of  putrefaction  may  be  obtained  from  bur  cuttings 
in  cases  of  moist  gangrene  only.     This  must  be  differentiated  from 

the  odor  of  decayed  dentine,  which  usu- 
ally also  has  an  acid  character. 

In  case  of  partial  death  of  the  pulp 
not  discoverable  by  the  tests  given  above, 
a  fine,  sharp  probe  passed  into  contact 
with  the  pulp  remnant  will  demonstrate 
its  vitality. 
Skiagraph  of  unfilled  root  canals       Treatment.     If  scptic  matter  be  intro- 

with  large   mass  of  filling  material      -,  ,  .    i        ,  .  ....  < 

built  in  over  them.   (Price.i)  cluccd   a    Violent  pericementitis  may  be 

lighted  up;  but  if  aseptic  precautions  be 
employed  in  opening  the  canal,  and  this  be  kept  under  the  influence 
of  a  germicide,  such  as  5  per  cent,  formaldehyde  or  sodium  dioxide, 
the  root  may  be  filled  by  the  immediate  method— r.  e.,  when  opened 
and  sterilized  it  is  to  be  dried  and  then  moistened  with  eucalyptol 
and  the  excess  of  this  removed;  previously  prepared  cones  of  tem- 
porary stopping  are  then  packed  into  the  root.  The  method  of 
moistening  the  canal  with  Forma-Percha  and  then  placing  the  cones, 
or  the  use  of  cotton,  silk,  or  asbestos  fibres  saturated  with  Forma- 
Percha  (see  p.  435),  has  all  the  advantages  of  the  temporary  anti- 
septic filling  with  the  added  merit  of  permanency  if  the  indications 
declare  a  success. 

A  temporary  filling  of  pink  base-plate  gutta-percha  is  to  be  inserted 
in  the  crown  cavity  until  all  irritation,  if  any,  subsides. 

Slight  aseptic  apical  irritation  may  be  anticipated  as  a  matter  of 
precaution  by  the  use  of  iodine  as  a  counterirritant  at  the  time  of  root 
filling.  (See  p.  387.)  Such  irritation  is  either  mechanical  or  due  to 
the  chemical  substances  used. 


MOIST  GANGRENE  OF  THE  PULP. 

Definition.     By  moist  gangrene  of  the  pulp  is  meant  death  of  pulp 
tissue  en  masse  and  its  subsequent  decomposition  by  the  action  of 

i  Items  of  Interest,  1901. 


MOIST  GANGRENE  OF  THE  PULP. 


447 


Fig.  407. 
Pigment.      Sulphur  +  hfemoglobin. 


putrefactive  agencies.  As  putrefactive  decomposition  is  the  essential 
feature  in  these  cases,  and  that  which  gives  the  process  its  pathological 
significance,  the  causes,  nature,  effects,  and  treatment  of  putrefactive 
decomposition  of  the  pulp  are  included  under  this  sub-heading. 

Causes.  The  causes  of  moist  gangrene  are  such  as  may  cause  the 
death  of  the  pulp  and  its  subsequent  decomposition  by  bacteria. 
Without  bacteria  moist  gangrene  cannot  occur.  Among  these  the 
bacillus  gangrense  pulpse  (Arkovy)  figures  prominently.  Four  types 
of  cases  are  seen:  (1)  in  teeth  apparently  sound;  (2)  in  teeth  filled, 
but  the  canals  not  treated — i.  e.,  death 
of  the  pulp  has  occurred  after  filling; 
(3)  in  teeth  filled  with  canals  partly 
filled;  (4)  in  teeth  having  open  cavi- 
ties and  canals. 

In  the  first  type  of  cases  the  bacteria 
may  enter  by  way  of  the  blood  chan- 
nels, but  it  is  not  improbable  that 
slight  cracks  or  histological  defects  in 
the  enamel  may  admit  to  the  dentinal 
tubules  the  necessary  bacteria,  or  that 
they  may  gain  entrance  by  way  of  the 
cementum  and  dentine  at  the  neck  of 
the  tooth.     (See  Caush's  tubes.) 

A  case  presenting  some  analogy  to 
these  teeth  is  that  of  an  egg  with  ap- 
parently perfect  shell,  but  in  which 
intense  decomposition  has  occurred. 

Many  of  these  teeth  do  not  develop 
abscesses  even  after  the  tooth  has  be- 
come dark  in  color.  If  the  dentine  be 
exposed  as  at  the  incisal  edge  the  ab- 
scess may  develop. 

In  the  filled  cases  crevices  about 
crown    and   root  fillings  may  admit 

bacteria,  which  may  pass  through  the  tubules  of  even  secondary 
dentine  in  some  amount.  On  the  other  hand,  it  is  irrational  not  to 
admit  the  possibility  of  an  infection  via  the  circulation. 

In  cases  of  obvious  pulp  infection  beneath  fillings — e.  g.,  suppura- 
tion of  the  pulp — the  bacteria  necessary  are  in  situ. 

In  the  open  cases  the  infection  obviously  arises  from  the  mouth. 


CO9,  NH3 ; 
H.O  and  HjS 


Aromatic  and 
fatty  prod- 
ucts. 


Ptomains. 


Peptones. 


Diagram  illustrating  the  more  complete 
decomposition  of  the  pulp  at  its  coronal 
end. 


448 


GANGRENE  OF  THE  PULP. 


Pathology  and  Morbid  Anatomy.  The  pulp  being  wholly  or  partly 
dead  from  any  cause  whatever,  saprophytic  bacteria  gain  access  to  it 
and  the  serial  decomposition  it  undergoes  is  in  exact  correspondence 
with  that  of  moist  gangrene  or  putrefaction  in  other  localities. 


Fig.  409. 


Fig.  410. 


Fig.  411. 


'e^ 


Fig.  413. 


Fig.  414. 


lj{U- 


«'//; 


Fig.  415. 


,%  f  -\ 


V    //      M 


In  this  serial  decomposition  albuiriinous  substances  are  first  trans- 
formed into  peptones  and  allied  substances,  some  of  them  being  very 
toxic.  Compound  ammonias,  known  as  ptomains,  or  animal  alkaloids, 
are   probably   next   formed.      Next   the   nitrogenous    bases — leucin. 


MOIST  GANGRENE  OF  THE  PULP.  449 

tyrosin,  and  the  amins  (methyl,  ethyl,  and  propyl) — make  their'appear- 
ance,  together  with  organic  fatty  acids.  Next  aromatic  products,  indol, 
phenol,  cresol,  etc.,  and  finally  hydrogen  sulphide,  ammonia,  carbon 
dioxide,  and  water.  By  alternating  processes  of  hydration,  reduction, 
and  oxidation,  bodies  of  increasing  simplicity  of  chemical  composition 
are  formed.^ 

Miller^  found  in  the  deepest  portions  of  the  degenerating,  putrefying 
pulps,  where  inflammation  and  suppuration  were  in  progress,  a  pre- 
ponderance of  small  cocci  and  diplococci,  and  proceeding  toward  the 
open  pulp  chamber  an  increasing  number  of  large  cocci,  several  forms 
of  bacilli,  vibrios,  and  other  spirillse,  spirochsetse,  and  long  thread 
forms  (Figs.  408  to  415).  Figs.  414  and  415  are  from  the  same  pulp;: 
Fig.  415  was  taken  from  the  radicular  portion  of  a  pulp  which  was 
alive  and  suppurating;  Fig.  414  was  from  the  putrid  crown  portion^ 
Miller  found  that  bacteria  of  pulp  putrefaction  cultivated  in  gelatin,, 
with  and  without  the  access  of  air,  exhibited  a  difference  in  the 
poisonous  properties  of  their  products.  Those  developed  with  free 
access  of  air  produced  stronger  reaction,  and  more  extensive  sup- 
puration than  those  developed  without  the  access  of  air. 

Arkovy,^  in  an  examination  of  43  cases  of  chronic  apical  abscess, 
pulp  gangrene,  etc.,  found  the  bacillus  gangrense  pulpse  present  in  41; 
the  S.  pyogenes  aureus  in  15;  S.  pyogenes  albus  in  8;  S.  pyogenes 
citreus  in  2;  S.  pyogenes  in  10,  and  B.  pyocyaneus  in  4. 

He  found  the  bacillus  gangrense  pulpse  in  mouths  free  of  caries  as 
well  as  in  mouths  containing  carious  teeth,  and  established  the  fact 
that  it  is  pleomorphous  (bacillus  and  coccus  form). 

He  inoculated  healthy  pulps  with  this  bacterium  and  found  that  in 
pure  culture  it  produced  total  gangrene  without  suppuration;  while 
mixed  cultures,  and  even  the  mixed  pleomorphic  forms  of  the  same 
bacillus,  produced  chronic  pulpitis. 

On  gelatin  cultures  a  putrid,  cheese-like  odor  was  perceptible.  The 
germ  is  subject  to  the  antiseptic  effects  of  strong  acids,  alkalies,  carbolic 
acid,  and  tincture  of  iodine,  which  explains  in  part  the  success  of  the 
treatment  hereinafter  mentioned. 

Arkovy's  demonstration  seems  a  satisfactory  explanation  of  cases 
of  quiet  death  of  pulps  under  fillings. 

The  hydrogen  sulphide  combines  with  the  iron  in  the  haemoglobin 
of  the  red  blood  corpuscles,  producing  ferric  sulphide  which,  entering 

1  Ziegler,  General  Pathology.  *  Dental  Cosmos,  1894. 

3  Synopsis  by  Soderberg,  Dental  Cosmos,  1899. 

29 


450  GANGRENE  OF  THE  PULP. 

the  tubules,  stains  the  dentine  a  slaty-gray  or  bluish-black  color. 
Other  derivatives  of  haemoglobin  may  be  responsible  for  the  yellowish- 
brown  discoloration  often  seen  in  cases  in  which  bacteria  have  not 
reached  the  pulp  until  long  after  pulp  death.  The  color  is,  there- 
fore, not  due  to  the  presence  of  hydrogen  sulphide. 

Fig.  407  is  a  diagram  illustrating  these  changes;  it  being  assumed 
that  the  decomposition  is  most  advanced  at  the  crown  portion  of  the 
pulp,  owing  to  the  entrance  of  bacteria  at  that  point. 

In  the  early  stage  of  the  process  the  gangrenous  pulp  resembles 
a  yellowish  mass  of  sloughing  tissue,  which  can  be  easily  removed. 
In  the  later  stages  it  is  more  decomposed,  and  yields  to  the  broach. 
In  the  final  stages  nothing  but  fluid,  or  even  an  almost  dry  canal, 
may  be  found.  This  last  condition  must  not  be  confounded  with  dry 
gangrene.  If  fluid,  or  odor  without  fluid,  be  present  the  case  is  one 
of  moist  gangrene. 

Symptoms.  As  a  rule,  the  tooth  presents  at  least  an  opacity  upon 
transmission  of  light,  but  usually  has  the  bluish  or  brownish  discolor- 
ation mentioned,  most  marked  at  the  cervical  third  of  the  crown  and 
most  noticeably  upon  the  lingual  side.  There  is  an  absence  of  response 
to  thermal  and  electric  tests.  Occasionally  the  patient  complains  of 
a  bad  taste  in  the  region  of  the  tooth.  This  is  due  to  slow  leakage. 
The  symptoms  of  septic  apical  pericementitis  may  be  localized  about 
the  apex  of  the  tooth,  or  at  times  the  pain  of  incipient  pericementitis 
may  be  reflected  or  a  history  of  apical  abscess  may  be  obtained,  con- 
firmed by  the  presence  of  a  fistula.  Occasionally  the  patient  complains 
of  apical  pain  upon  passing  from  a  warm  to  a  cold  atmosphere  and 
vice  versa.  Upon  drilling  out  a  filling  the  odor  of  putrefaction  may 
be  clearly  noticed,  even  before  the  entrance  of  the  canal.  The  odor 
of  the  bur  cuttings  is  diagnostic  in  less  pronounced  cases.  The  mal- 
odorous gases  may  be  present  in  quantity  without  acute  symptoms  of 
pericementitis. 

It  is  presumptive  that  in  some  cases  these  gases  gradually  escape 
through  the  tubules  and  by  way  of  leaks  about  the  fillings,  a  fact 
which  may  act  favorably  by  preventing  accumulation  and  the  form- 
ation of  an  apical  abscess. 

A  confusing  condition  clinically  is  found  where  one  half  of  a  pulp 
has  died  and  undergone  decomposition,  as  in  molars,  the  other  half 
remaining  vital,  although  the  seat  of  infection  and  inflammatory 
action.  So  far  may  this  condition  go,  that  abscess,  acute  or  chronic, 
may  be  present  upon  the  root  of  one  tooth  long  before  the  second 


MOIST  GANGRENE  OF  THE  PULP.  45 1 

segment  of  the  pulp  has  succumbed.  The  diagnosis  of  such  cases  is 
made  by  the  Hght  test,  by  obtaining  the  painful  reaction  to  heat  and 
perhaps  to  electricity,  and  usually  some  tenderness  upon  percussion 
upon  some  particular  portion  of  the  tooth;  upon  opening  the  tooth 
the  peculiar  condition  described  is  found. 

In  one  case  of  a  lower  molar  with  a  fistula  related  with  the  distal 
root,  I  found  the  pulp  apparently  vital  upon  entering  the  pulp  chamber 
with  a  bur  at  a  point  about  midway  between  the  horns.  There  was 
apparently  a  persistence  or  hypertrophy  of  the  pulp  bulb  attached  to 
the  mesal  filaments.  The  distal  canal  was  found  to  contain  only  the 
fluid  remains  of  a  pulp  filament. 

In  cases  seen  at  the  right  time  the  bulbal  half  of  a  pulp  may  be 
gangrenous  without  positive  putrefaction,  while  the  apical  half  is  still 
vital. 

J.  H.  McQuillen^  recorded  a  case  of  longitudinal  fracture  of  a 
bicuspid  tooth  extending  from  the  sulcus  to  the  bifurcation  of  the 
roots,  and  which  was  apparently  due  to  the  expansion  of  the  gases 
of  decomposition.  Poinsot^  records  a  similar  case  and  states  that 
several  teeth  containing  decomposed  pulps  confined  in  a  glass  tube 
caused  the  latter  to  break. 

Observations  previous  to  that  of  McQuillen  have  recorded  a  sound, 
as  of  an  explosion,  to  have  occurred  simultaneously  with  the  fracture 
of  the  tooth.  I  have  looked  all  my  professional  life  for  such  a  case, 
but  have  never  been  able  to  ehminate  the  possibility  of  fracture  from 
ordinary  causes. 

Treatment.  The  general  principle  of  treatment,  in  all  cases  present- 
ing without  symptoms  of  apical  pericementitis,  is  the  disinfection  of 
canals,  the  removal  of  all  decomposed  and  decomposing  pulp  tissue, 
prevention  of  infection  of  the  pericementum,  and  hermetical  sealing 
of  the  apex  and  body  of  the  canal  by  means  of  appropriate  root  filHngs. 

In  all  cases  the  imminent  danger  and  that  to  be  guarded  against  is 
to  avoid  mechanically  carrying  a  portion  ever  so  minute  of  infective 
material  past  the  apical  foramen.  This  implies  either  great  dexterity, 
or  the  use  of  a  germicide  which  shall  sterilize  the  pulp  tissue  before 
the  attempt  is  made  to  remove  it.  Should  any  pass  through,  it  must 
be  sterilized  by  strong  germicides  passed  after  it. 

There  are  three  good  methods  of  accomplishing  the  treatment  of 
gangrenous  pulps  to  be  chosen  from,  according  to  the  access  obtainable 

1  Dental  Cosmos,  1871.  ^  Ibid.,  1901. 


452  GANGRENE  OF  THE  PULP. 

to  the  apices  of  canals.  The  first  is  an  "immediate"  method.  The 
tooth  is  to  be  placed  under  rubber-dam  and  the  crown  sterilized,  or 
the  mouth  is  to  be  sterilized  by  the  use  of  a  germicidal  mouth-wash 
— e.  g.,  a  strong  solution  of  potassium  permanganate,  meditrina,  or  a 
wash  representing  1 :  2000  mercuric  chloride,  preferably  in  hydrogen 
dioxide. 

The  tooth  is  then  to  be  carefully  opened  until  all  the  canals  can  be 
readily  entered.  This,  as  a  rule,  implies  a  free  opening  from  the 
occlusal  surface  in  direct  line  with  the  canal,  though  a  slight  indirect- 
ness, if  the  entrance  be  free,  is  often  admissible  as  conservative  of  tooth 
structure.  The  opening  must  admit  of  thorough  work,  even  if  the 
tooth  be  somewhat  weakened.  A  finely  pointed  broach,  made  by 
filing  down  an  old  Donaldson  cleanser,  is  moistened  by  drawing  it 
through  a  drop  of  water.  It  is  then  drawn  through  dry  sodium  dioxide, 
several  small  portions  of  which  have  been  placed  upon  a  glass  slab. 
The  adherent  material  is  carried  to  the  canal,  which  may  be  left  in 
a  moist  condition,  and  gently  insinuated  into  it. 

Reaction  with  the  water  produces  sodium  hydrate,  which  dissolves 
all  organic  matter,  and  hydrogen  dioxide,  which  by  a  further  reaction 
liberates  nascent  oxygen.^  This  first  application  may  be  carried  as 
far  as  may  be  done  without  pressure.  If  the  canals  be  constricted 
they  may  be  slightly  enlarged  at  their  mouths  with  Gates-Glidden 
drills,  etc.  (See  p.  432.)  More  sodium  dioxide  is  then  applied  and  after 
its  action  the  canal  may  be  partially  freed  of  debris  by  means  of  a 
stream  of  water,  and  a  fine  Donaldson  cleanser  acting  at  the  same  time. 
The  canals  are  partly  dried  and  more  sodium  dioxide  deeply  inserted. 

A  small,  short,  Kerr  or  Downie  broach,  a  form  of  tapering  twist  drill, 
is  now  used  to  enlarge  the  apical  portion  of  the  root,  following  which 
either  the  Callahan  method  of  enlargement  by  sulphuric  acid  and 
the  Donaldson  cleanser  (see  p.  433),  or  enlargement  by  Gates- 
Glidden  or  Moray  drills  may  follow  as  indicated.  These  latter  should 
be  avoided  if  the  roots  are  curved. 

1  Schrier's  alloy  of  metallic  sodium  and  potassium  (kalium-natrium)  may  be  substituted, 
but  with  no  distinct  advantage,  as  by  reaction  with  water  an  explosion  occurs,  an  atom  of  the 
hydrogen  of  the  water  molecule  taking  fire  while  sodium  and  potassium  hydrate  (caustic 
sodium  and  potassium)  are  formed.  Could  the  heat  be  produced  within  the  canal  there  would 
be  advantage,  but  it  occurs  only  at  the  canal  mouth  or  a  short  distance  beyond.  Sodium 
dioxide  in  the  dry  state  should  not  come  into  contact  with  carbolic  acid  or  essential  oils,  as  an 
explosion  may  occur;  when  water  is  used  the  sodium  dioxide  is  decomposed  by  it  and  the 
danger  is  removed.  Instead  of  the  sodium  dioxide  method  a  strong  solution  of  potassium  per- 
manganate may  be  used.  The  discoloration  may  be  removed  by  the  use  of  a  saturated  solution 
of  oxalic  acid  in  25  per  cent,  hydrogen  dioxide.  In  certain  cases  it  may  be  left  without  de- 
colorizing. 


MOIST  GANGRENE  OF  THE  PULP.  453 

A  Swiss  broach  nicely  tempered  to  a  pigeon-blue  color  in  a  test-tube 
is  useful  for  the  reaming  of  fine  roots. 

If  the  apical  foramen  be  open,  or  can  be  opened,  the  dilute  sodium 
hydrate  may  be  permitted  to  pass  through  into  the  apical  tissue  to 
destroy  any  putrid  matter  possibly  forced  through.  Meditrina  is  less 
irritating.  A  good  method  is  to  apply  sodium  dioxide  for  five  minutes, 
and  then  25  per  cent,  ethereal  pyrozone  or  meditrina  for  ten  minutes. 
If  the  foramen  be  impossible  of  exploration  several  methods  of  steril- 
ization are  available: 

1.  The  25  per  cent,  ethereal  solution  of  pyrozone  may  be  placed  in 
the  canals  on  cotton,  upon  the  theory  that  it  will  penetrate  the  slight 
portion  of  unexplored  root  canal  and  the  tubules  of  the  dentine  as  in 
bleaching.  Its  action  will  be  favored  by  the  slight  amount  of  sodium 
dioxide  previously  used. 

2.  A  zinc  probe  may  be  introduced  into  the  canaj|  and  the  positive 
pole  of  the  cataphoric  apparatus  applied  to  it.  Oxy chloride  of  zinc 
is  formed  at  the  canal  apex,^  and  penetrates  to  the  soft  tissues, 
sterilizing  everything. 

3.  Nitrate  of  silver  may  be  forced  by  cataphoresis  into  the  canal, 
according  to  the  method  advocated  by  Bethel,  confining  the  opera- 
tion to  posterior  teeth  because  of  the  discoloration  produced.  The 
crown  cavity  is  to  have  its  walls  covered  with  wax  or  varnish  to  prevent 
the  passage  of  the  silver  nitrate  into  the  crown  dentine;  the  canal  is 
pumped  full  of  a  silver-nitrate  solution  (25  per  cent,  to  75  per  cent.), 
a  pellet  of  cotton  containing  the  same  solution  is  wrapped  around  the 
positive  electrode  of  a  cataphoric  apparatus,  the  current  is  applied, 
and  the  silver  solution  is  driven  into  all  of  the  tortuosities  of  the  canal 
(Fig.  416).  The  silver  combines  with  the  contents  of  the  dentinal 
tubuli,  forming  silver  albuminate;  nitric  acid  is  formed  at  the  posi- 
tive pole  (the  electrode),  giving  an  acid  reaction  to  the  canal  con- 
tents; the  acid  is  to  be  neutralized  with  ammonia.  Unless  a  very  high 
voltage  be  applied,  the  silver  does  not  penetrate  the  dentine  to  any 
considerable  depth,  and  it  is  not  desired  to  have  it  do  so.  Credo's 
experiments  indicate  that  metallic  silver  acts  as  an  antiseptic  by  being 
oxidized  by  bacterial  products,  the  argentic  oxide  being  afterward 
transformed  into  antiseptic  salts  of  silver  by  bacterial  waste  products, 
notably  by  lactic  acid,  silver  lactate  being  formed. 

Morton  has  suggested  the  driving  of  such  antiseptics  as  mercuric 

1  Ehein,  Items  of  Interest,  1897. 


454 


GANGRENE  OF  THE  PULP. 


chloride  in  hydrogen  dioxide  into  the  tubuH  and  canal  ends  by  the 
aid  of  the  cataphoric  current. 

F.  Milton  Smith  recommends  that  carbolic  acid  be  forced  into  the 
apical  tissue  by  the  method  used  in  pressure  anfesthesia  (see  p.  420) 
as  a  germicidal  agent  after  the  canal  is  cleansed. 

Dr.  J.  C.  Blair  introduced  the  method  of  vaporizing  iodoform 
lodged  in  a  special  receptacle  of  a  hot-air  bulb.  The  vapor  is  driven 
by  the  air  stream  into  the  dried  dentine.  The  method  is  successful, 
but  the  odor  generated  is  exceedingly  objectionable. 


Fig.  416. 


1.  Operated  on  in  the  mouth  with  a  50  per  cent,  solution  silver  nitrate.  Crown  cavity  pro- 
tected from  discoloration  by  a  thin  coating  of  melted  ^vax. 

2.  Operated  on  in  the  mouth  with  a  75  per  cent,  solution  silver  nitrate.  Crown  cavity  pro- 
tected with  wax. 

3.  Operated  on  in  the  mouth  with  75  per  cent,  solution  silver  nitrate. 

4.  Shows  perfect  lining  formed,  and  jDeneti-ation  of  the  silver  nitrate  into  the  dentinal  tubuli. 

5.  Freshly  extracted  tooth  operated  on  outside  the  mouth.  The  cro'wn  and  roots  were  filled 
■with  decomposing  material  -^^'hich  -was  not  removed,  the  electrode  and  nitrate  being  applied  to 
the  surface ;  still  the  nitrate  permeated  the  canals.     Exposed  surfaces  of  both  canals  shown. 

6.  Operated  on  outside  of  mouth.     Foramen  on  inside  of  root. 

7.  Shows  penetration  in  flat  root  with  constricted  and  branching  root  canal.  Could  not  get 
broach  more  than  one-eighth  inch  into  canal. 

8.  Operated  on  outside  of  mouth  for  twelve  minutes,  attempting  to  force  the  .silver  nitrate 
through  foramen  of  root. 

9.  Shows  returning  branch  of  canal  that  might  easily  be  left  unfilled.     (Bethel.) 

The  same  object  may  be  attained  by  introducing  a  saturated  solu- 
tion of  iodoform  in  alcohol  after  complete  desiccation  of  the  root 
dentine.^ 

Complete  carbonization  of  the  contents  of  a  canal  by  means  of  a 
suitable  electrocautery  or  Evans  root  drier  is  a  rapid  and  satisfactory 
method  of  sterilization. 

The  principle  involved  in  immediate  sterilization  is  the  destruction 
of  all  septic  matter  within  the  canal  and  beyond  the  apex  at  the  first 
sitting. 

After  the  canal  disinfection  is  accomphshed  by  one  or  more  of  the 
various  immediate  means  suggested,  its  walls  should  be  desiccated 


'  Register. 


MOIST  GANGRENE  OF  THE  PULP.  455 

and  made  absorbent  by  means  of  hot  air,  then  moistened  with  eucalyptol 
or  "  Forma-Percha  "  and  a  root  filling  of  temporary  stopping  or  gutta- 
percha packed  in.  If  aristol  be  added  to  these  the  effect  is  increased. 
Cotton  and  "  Forma-Percha  "  make  a  readily  removable  filling  suit- 
able to  cases  in  which  some  doubt  exists.  I  have  had  excellent  results 
in  molars  with  this  material.     (See  p.  437.) 

A  temporary  filling  of  base-plate  gutta-percha  is  then  placed  in  the 
crown  cavity  as  a  test  filling,  or,  in  case  of  need,  the  filling  may  be 
inserted. 

Any  apical  irritation  may  be  attributed  to  the  disinfectant  and  be 
treated  by  counterirritation  or  the  counterirritant  may  be  applied 
as  a  precaution  at  the  time  of  operation.  Refrigeration  of  the  gum 
over  the  root  by  means  of  ethyl  chloride  is  a  valuable  means  of  reduc- 
ing inflammation  in  these  cases.  This  traumatic  irritation  is  often 
mistaken  for  acute  septic  pericementitis.  Any  irritation  not  too 
severe  is  to  be  considered  as  due  to  non-septic  causes  and  treated 
accordingly.  A  few  of  these  cases  may,  of  course,  result  in  failure 
owing  to  imperfection  in  the  application  of  the  method.  The  great 
majority  of  cases  are  successful. 

As  a  precaution  against  possible  infection  of  the  apical  space  while- 
cleansing  the  root  some  operators  prefer  to  open  the  pulp  chamber 
and  seal  therein  a  pellet  of  cotton  containing  a  10  per  cent,  solution 
of  formaldehyde;  twenty-four  hours  later  the  canal  cleansing  is  under- 
taken. The  formaldehyde  gas  expands  at  body  temperature  and 
penetrates  the  pulp  tissue,  sterilizing  it. 

Geranium-formoP  may  be  substituted  and  has  the  following  com- 
position : 

Jt— Formic  aldehyde,  40  parts. 

Essence  of  geranium  (redistilled),  20      " 

Alcohol,  80  degrees,  40      " 

Phenol-camphor  may  be  made  by  rubbing  together  in  a  mortar 
equal  parts  of  gum  camphor  and  crystal  carbolic  acid.  An  oily  liquid 
is  formed. 

Endelman^  modifies  this  as  follows: 

9^ — Formalin  (40  per  cent,  aqueous 

formaldehyde  solution),  n\x. 

Oil  of  geranium,  Sj. 

If  confidence  in  the  suitability  of  immediate  root  filling  in  any  case 
be  lacking,  the  canal  may  after  desiccation  be  dressed  mth  cotton 

1  Dental  Cosmos,  1904. 

2  Andr(5  and  de  Marion,  L'Odontologie.     Abstract  by  International  Dental  Journal,  1901. 


456  GANGRENE  OF  THE  PULP. 

saturated  with  a  diffusible  antiseptic,  such  as  5  per  cent,  formaldehyde 
or  geranium-formol,  iodoform  or  hydronaphthol  in  alcohol,  creosote, 
phenol-camphor,  etc.,  and  the  cavity  sealed  for  a  few  days.  The 
oils  of  cassia  and  cloves  are  apt  to  cause  discoloration  of  the  dentine 
and  should  be  avoided  in  anterior  teeth.  The  supervention  of  acute 
septic  pericementitis  is  an  indication  of  failure.  This  may  be  denomi- 
nated the  "tentative"  method. 

The  withdrawal  of  the  cotton  dressing  in  the  tentative  method 
should  be  done  under  aseptic  precautions.  There  may  be  found  no 
collection  upon  the  cotton.  In  such  case  a  fresh  twist  on  a  Swiss 
broach  should  be  passed  to  the  apex  to  determine  its  condition.  If 
nothing  be  found  the  root  may  be  dried  and  filled  unless  odor  be 
present,  when  the  root  should  be  resterilized  before  filling  or  the  dress- 
ing renewed. 

Active  hemorrhage  may  ensue  or  serum  may  ooze  from  the  apical 
tissue.  This  may  be  checked  with  25  per  cent,  pyrozone,  adrenalin 
chloride  1 :  1000,  or  preferably  deliquesced  zinc  chloride,  and  the  root 
filled. 

If  a  pus  flow  follow  the  removal  of  the  temporary  dressing  and  be 
but  slight,  the  pyrozone  or  zinc  chloride  (or  both)  should  be  used 
and  the  root  filled.  The  condition  is  one  of  apical  abscess  without 
fistula  and  is  often  amenable  to  immediate  root  filling.  If,  however, 
this  be  not  considered  advisable  the  temporary  dressings  may  be 
renewed,  though  often  without  benefit.  Sometimes  a  thick,  glairy 
fluid  will  ooze  from  the  apical  tissue.  This  is  coagulable  lymph  and 
the  parts  require  treatment  in  the  same  manner  as  when  a  slight 
amount  of  pus  is  present.  The  principle  involved  in  the  departure 
to  an  immediate  method  of  treatment  is  based  upon  the  thorough 
sterilization  of  the  apical  tissue,  the  sealing  of  the  canal  to  prevent 
infection  from  the  mouth,  and  the  exclusion  of  effusions  from  the 
apical  tissue.  This  done,  the  apical  tissue  is  expected  to  care  for 
itself. 

In  order  to  prevent  apical  irritation  in  so  far  as  possible,  the  gum 
is  to  be  painted  with  ordinary  tincture  of  iodine  or  spotted  with  the 
dental  tincture  of  iodine,  both  lingually  and  buccally,  as  a  counter- 
irritant. 

9; — Iodine,  3iij. 

Alcohol,  Sj. 

Shake  frequently  for  a  week  or  two.     (Flagg.) 

If  infection  of  the  apical  tissue  by  any  chance  ensue,  either  as  the 
result  of   the  operation  of  canal  cleansing  or  previous  to  operative 


MOIST  GANGRENE  OF  THE  PULP.  457 

interference,  the  disease  known  as  septic  apical  pericementitis  is 
established. 

Pericementitis  following  the  opening  of  teeth  containing  gangrenous 
pulps  has  been  explained  upon  the  ground  that  the  bacteria  in  the 
absence  of  free  admission  of  oxygen  have  lost  their  virulence,  which 
is  restored  when  the  air  is  admitted.  It  is  quite  likely  that  either 
this  is  true  or  that  extraneous  bacteria  are  introduced  during  the 
course  of  treatment. 

In  case  of  partial  moist  gangrene  in  which  a  portion  of  a  filament 
is  gangrenous  and  the  balance  of  it  vital,  or  in  which  one  root  filament 
is  dead  and  the  other  vital,  the  treatment  must  be  varied  to  suit  the 
requirements.  The  dead  portion  is  removed  as  described  and  the 
living  portions  treated  as  ulcerated  pulps  (which  see,  p.  405). 

In  a  few  cases  the  continuity  of  the  canal  has  been  lost  because  it 
has  become  involved  in  caries  upon  one  side  of  the  root.  To  remedy 
this  if  the  root  be  still  salvable  the  cavity  should  be  excavated  and 
then  a  tapering  probe  run  through  the  tap  in  the  crown  and  into 
the  apical  portion  of  the  root  canal.  Around  this  an  amalgam  filling 
may  be  built.  The  probe  is  then  withdrawn,  leaving  a  canal  in  the 
amalgam  through  which  later  the  canal  may  be  treated  and  filled. 

Moist  Gangrene  of  Pulps  of  Temporary  Teeth.  The  same  con- 
siderations pertain  to  moist  gangrene  of  the  pulps  of  temporary  teeth, 
but  as  the  roots  are  resorbed  to  some  extent  or  are  to  be  resorbed, 
the  root  filling  should  be  of  such  a  character  as  to  permit  its  resorp- 
tion. Probably  a  combination  of  paraffin  and  aristol  will  best  fulfil 
the  indications. 

If  the  roots  be  much  resorbed  it  is  better  to  use  a  material  which 
will  permit  venting  of  the  tooth  if  necessary.  The  canals  and  pulp 
chamber  may  be  filled  with  a  combination  of  vaselin  and  aristol  and 
this  covered  by  a  filling.  If  trouble  arise  a  spear  drill  is  driven  into 
the  pulp  cavity  from  a  point  near  the  cervix. 

At  an  age  when  the  permanent  tooth  will  shortly  thereafter  erupt, 
extraction  of  the  temporary  tooth  is  often  to  be  preferred  to  treatment. 

Root-canal  Work  in  Cases  of  Gangrenous  Pulps  Involving 
Future  Consideration.  In  some  cases  of  doubtful  root  sterilization 
or  filling,  and  in  which  crowning  by  means  of  dowelled  crowns  is  a 
necessity,  provision  may  be  made  for  future  relief  or  treatment  by 
the  employment  of  one  of  two  excellent  methods  of  procedure: 

1.  Kirk  has  suggested  that  the  post  and  band  of  a  Richmond  crown 
be  painted  while  warm  with  a  solution  of  gutta-percha  in  chloroform. 


458  GANGRENE  OF  THE  PULP. 

The  solvent  evaporates,  leaving  a  coating  of  gutta-percha.  The  crown 
is  then  set  with  cement.  By  warming  the  crown  with  a  hot  crown- 
setting  tool  (How)  or  forceps,  it  may  be  removed  with  ease.  The 
crown  may  be  set  with  gutta-percha  alone. 

2.  Girdwood  (Edinburgh)  has  suggested  root  intubation,  the  tube 
being  closed  at  the  end  with  temporary  stopping  and  then  set  with 
cement.  Immediately  thereafter  the  temporary  stopping  and  soft 
cement  are  removed  with  Donaldson  cleansers,  leaving  the  root  lumen 
free  to  the  apical  foramen  or  root  filling.  The  tube  and  canal  are 
then  treated  as  a  continuous  root  canal  would  be.  The  idea  is  also 
applied  to  a  Richmond  or  all-porcelain  crown,  the  tube  being  allowed 
to  extend  through  the  solder  backing,  to  be  later  filled  as  desired. 


SECTION   V. 

DISEASES  OF  THE  PERICEMENTUM. 


CHAPTER   XX. 

SEPTIC  APICAL  PERICEMENTITIS  (ACUTE). 

Classification.  The  dental  periosteum  and  ligament,  or  the  peri- 
cementum, is  the  seat  of  numerous  nutritive  and  functional  disturb- 
ances, which  may  be  grouped,  according  to  their  causes,  into  septic 
and  non-septic. 

The  term  pericementitis  has  been  indiscriminately  applied  to  all 
affections  of  the  pericementum,  and  in  some  cases  erroneously,  for  in 
not  all  affections  of  this  structure  do  the  phenomena  of  inflammation 
appear.  However,  most  of  the  acute  and  chronic  degenerations  are 
accompanied  by  evidences  of  inflammation. 

Bodecker's  division  of  the  affections  of  the  pericementum  into  puru- 
lent and  non-purulent  is  misleading.  Cases  may  be  due  to  septic 
causes  without  pus  formation ;  pus  formation  represents  but  one  form 
of  sepsis. 

The  most  convenient  clinical  classification  of  these  disorders  is  that 
offered  by  G.  V.  Black  :^  first,  diseases  of  the  pericementum  beginning 
at  the  apex  of  the  root;  secondly,  those  beginning  at  the  gum  margin; 
thirdly,  those  beginning  in  some  intermediate  portion  of  the  peri- 
cementum. These  may  again  be  divided,  according  to  their  causes, 
into  septic  and  non-septic.  Another  clinical  classification  would  be 
into  localized  and  general  disturbances — another  into  acute  and 
chronic. 

Evidences  of  Pericemental  Disturbance.  It  was  noted  in  the 
study  of  the  diseases  of  the  dental  pulp  that  the  diagnostic  signs  of 
pulp  disturbance  were  exaggerated  or  diminished  response  to  thermal 
stimuli;  reflected  instead  of  localized  pains;  and,  except  in  rare  cases 

1  American  System  of  Dentisti-y,  vol.  i. 


460  DISEASES  OF  THE  PERICEMENTUM. 

of  advanced  degeneration,  no  tenderness  upon  percussion.  Disturb- 
ances of  the  pericementiun  are  accompanied  by  entirely  different 
symptoms  which  serve  to  distinguish  between  them  and  diseases  of 
the  pulp.  They  are,  in  general,  tenderness  upon  percussion.  As 
shown  by  Black,^  the  pericementum  is  the  touch  organ  of  the  tooth* 
its  tactile  organ,  through  which  a  tooth  locates  force  applied  to  the 
tooth.  The  pains  of  pericemental  disturbance  are,  therefore,  in  the 
majority  of  cases,  exactly  localized,  instead  of  not  being  localized  as 
in  the  case  of  the  pulp.  A  tooth  tender  upon  percussion  has  its  peri- 
cementum as  the  seat  of  disturbance.  Most  cases  of  pericemental  dis- 
eases are  accompanied  by  vascular  reactions  ranging  from  an  increased 
blood  flow  or  grades  of  hj^ersemia  to  pronounced  inflammation,  and 
have  the  corresponding  symptoms.  The  increased  volume  of  the  peri- 
cementum causes  the  protrusion  and  loosening  of  the  tooth,  heightened 
sensitivity  being  the  accompaniment.  As  the  vascular  supply  of  the 
pericementum  and  that  of  the  gum  are  in  a  degree  collateral  (see 
p.  152),  evidences  of  vascular  engorgement  are  seen  in  the  gum 
overlying  the  affected  tooth.  Owing  to  the  altered  density  of  the 
parts  surrounding  the  tooth  root,  percussion  upon  the  tooth  elicits 
a  different  sound  from  that  observed  in  health— the  sound  is  dull. 
The  general  symptoms  of  pericemental  affections  are,  therefore, 
tenderness  upon  percussion  and  a  dull  percussion  note,  more  or  less 
protrusion  and  looseness  of  the  tooth,  and  a  deepening  of  the  local 
gum  color. 

DISEASES  OF  THE  PERICEMENTUM  BEGINNING  AT  THE  APEX. 

Diseases  of  the  pericementum  beginning  at  the  apex  of  the  root  are 
of  two  classes,  septic  and  non-septic.  The  septic  cases  are  almost 
invariably  the  sequel  to  diseases  of  the  pulp,  namely,  suppuration  and 
gangrene;  or  arise  in  consequence  of  infection  through  the  canals  of 
pulpless  teeth.  The  non-septic  cases  are  due  to  mechanical  and 
chemical  irritants,  and  in  rare  cases  to  undiscovered  causes. 

Acute  Septic  Apical  Pericementitis — Acute  Alveolodental 
Abscess.  Definition.  By  septic  apical  pericementitis  is  meant  an 
inflammation  of  the  apical  pericementum  due  to  the  entrance  of  septic 
organisms  into  the  tissue  lying  in  the  apical  space. 

Causes,  The  most  common  causes  of  septic  apical  pericementitis 
are: 

1  American  System  of  Dentistry,  vol.  i. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  461 

1.  Septic  organisms  engaged  in  the  putrefaction  of  a  gangrenous 
pulp.  The  gases  and  toxic  products  evolved  by  the  process  also 
cause  much  irritation. 

2.  Pyogenic  organisms  engaged  in  the  production  of  suppuration 
of  the  pulp. 

3.  Septic  organisms  introduced  into  the  otherwise  aseptic  tissues 
of  the  apical  space  by  means  of  instrumentation  or  other  lack  of 
aseptic  precautions. 

4.  Infection  of  an  apical  space  by  an  abscess  arising  in  some  con- 
tiguous part  and  extending  in  the  direction  of  the  apical  space  under 
consideration. 

5.  Septic  infection  from  a  pyorrhoea  pocket  located  upon  the  side 
of  the  tooth  in  question,  the  deepest  portion  of  which  approximates 
the  apical  space. 

6.  Possible  infection  by  way  of  the  pericemental  tract  from  the 
gum  margin  or  by  way  of  the  circulation,  which  infection  may  cause 
a  pericemental  abscess  located  in  the  apical  tissue. 

The  last  two  conditions  would  be  septic  apical  pericementitis,  but  are 
to  be  considered  separately  as  pericemental  abscess.  (See  Pyorrhoea 
Alveolaris.)    As  a  cause  of  apical  abscess  it  is  rare,  but  has  been  seen. 

Apart  from  these  causes  infective  inflammation  of  apical  tissue 
does  not  seem  to  occur.  It  is  to  be  remembered  that  a  small  portion 
of  gangrenous  pulp  beneath  a  root-canal  filling  is  equivalent  to  an 
entire  gangrenous  pulp  as  a  cause  of  pericementitis.  The  vast  majority 
of  cases  occur  as  a  sequel  to  moist  gangrene  of  the  pulp,  either  before 
or  after  instrumentation  or  as  a  result  of  infection  of  the  apical  tissue 
by  instruments  either  unsterilized  or  reinfected  by  contact  with  the 
oral  fluids. 

The  organisms  found  in  acute  apical  abscesses  are  those  usually 
found  in  gangrenous  and  suppurating  pulps  and  in  a  certain  percentage 
of  even  healthy  mouths.  (See  p.  45.)  Schreier  found  the  diplo- 
coccus  pneumonias  in  fifteen  out  of  twenty  cases  examined.  He  also 
found  staphylococcus  pyogenes  albus  and  aureus,  and  occasionally 
streptococcus  pyogenes. 

Arkovy  found  the  bacillus  gangrense  pulpse  in  a  number  of  cases. 
(See  p.  449.)  These  are  virtually  the  same  organisms  that  are  found  in 
the  deeper  portions  of  a  suppurating  or  gangrenous  pulp :  this  fact  in 
itself  is  enough  to  show  the  continuity  of  infection  from  the  pulp  canal. 
It  is  a  well-known  clinical  fact  that  acute  outbreaks  of  septic  apical 
pericementitis  are  most  liable  to  occur  under  those  conditions  when 


462 


DISEASES  OF  THE  PERICEMENTUM. 


patients  "take  cold."  Schreier  points  out  that  these  atmospheric 
states  produce  a  bodily  condition  which  favors  the  development  of 
the  diplococcus  pneumonia,  and  finds  in  the  association  of  these 
factors  the  reason  why  this  diplococcus  should  be  pathogenic  in  the 
dental  condition. 

Pathology,  Morbid  Anatomy,  and  Symptoms.  The  Inflammatory 
Stage.  As  in  abscess  elsewhere  there  is  first  infection  by  pyogenic 
organisms  which  produce  the  phenomena  of  infective  inflammation 
within  the  substance  of  the  apical  tissue,  and  in  the  later  stages  in 
the  contiguous  tissues. 

Fig.  417. 


Showing  the  morbid  anatomy  of  septic  apical  pericementitis  (acute):  A,  pus;  B,  area  of 
dying  leukocytes ;  C,  septic  matter  in  root  canal ;  D,  excavation  of  process  (osteomyelitis); 
E,  swollen  periosteum  and  gum ;  F,  alveolar  bone :  G,  pericementum  at  edge  of  necrosis. 


Following  the  infection,  arterial  hypersemia  is  produced,  sensation 
is  exalted,  and  the  tooth  becomes  tender  upon  percussion;  but  if 
forcibly  pressed  upon — i.  e.,  if  the  arteries  be  compressed — the  hyper- 
semia is  momentarily  lessened  and  the  pressure  brings  a  sense  of 
relief.  At  this  stage  the  gum  over  the  apex  looks  normal,  but  may 
respond  to  pressure. 

Following  the  arterial  hypersemia  the  venous  obstruction  which 
ends  in  stasis  is  inaugurated,  and  diapedesis  of  leukoc}i:es  and  fibrinous 
exudation  into  the  intervascular  tissue  occurs.  The  fixed  cells  undergo 
proliferation. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS. 


463 


As  this  condition  of  inflammation  becomes  established  the  pain  due 
to  pressure  upon  the  sensory  nerves  becomes  of  a  \T!olent  throbbing 
character,  accompanied  by  a  sense  of  fulness.  The  swelling  of  the 
tissue  about  the  apex  of  the  root,  due  to  the  excess  of  fluid,  blood, 
leukocytes,  and  tissue  cells,  of  necessity  pushes  the  tooth  from  its  socket, 
so  that  it  feels  and  is  longer  than  the  other  teeth.  Moreover,  as  it  is 
bitten  upon  the  apical  tissue  is  further  irritated.  The  tooth  is  loosened 
and  percussion  induces  pain  and  elicits  the  dull  note  which  is  diag- 
nostic of  the  increase  of  bulk  in  the  pericementum.  The  color  of  the 
gum  over  the  root  becomes  deepened. 

First  Stage  of  Pus  Formation.  The  central  area  of  the  apical 
tissue — i.  e.,  that  next  the  apical  foramen — is  broken  down  into  pus. 


Acute  abscess  in  second  stage.  Tooth 
opened  at  6  for  treatment,  making-  a  blind 
abscess.     (Black.) 


some  of  which  enters  the  root 
canal  (Fig.  417,  A).  As  the  area 
of  pus  formation  widens,  all  of 
the  apical  tissue  is  liquefied 
(Figs.  418,  a;  419,  a). 

Second  Stage  of  Pus  For- 
mation. The  bone  cells  become 
involved  in  the  process  and  are 
destroyed  (osteitis).  The  throb- 
bing pain,  the  extrusion,  looseness,  and  dulness  to  percussion,  and  the 
inflammation  and  oedema  of  the  contiguous  tissues  are  marked.  The 
gum  is  widely  inflamed,  reddened,  and  swollen,  but  no  demarcation  of 
an  abscess  may  be  noted  upon  the  gum  at  this  stage.  The  membranes 
of  the  adjoining  teeth  become  irritated  and  hypersemic,  and  they  may 
exhibit  tenderness  upon  percussion  (Fig.  418). 


Acute  alveolar  abscess  of  a  lower  incisor, 
■wath  pus  cavity  between  the  bone  and  the 
periosteum:  a,  pus  cavity  in  the  bone  ;  6,  pus 
between  the  periosteum  and  bone ;  C,  lip  ;  d, 
tooth;  e,  tongue.     (Black.) 


464  DISEASES  OF  THE  PERICEMENTUM. 

Third  Stage  of  Pus  Formation.  The  pus  continues  to  form 
in  all  directions  until  the  bone  is  perforated  at  some  point — ?'.  e., 
usually  through  the  labial  alveolar  plate — that  being  the  thinnest  and 
most  readily  perforated.  The  periosteum  is  now  destroyed  and  the 
gum  tissue  directly  involved  as  a  boundary  to  the  pus,  which,  collecting 
beneath  it,  raises  it  into  a  distinctly  demarked  tumefaction  (Fig.  419,  b). 
The  pain  becomes  less  acute  owing  to  the  binding  resistance  of  the 
gum  being  less  than  that  of  the  bone.  At  first  the  swelling  is  hard, 
and  this  represents  a  mass  of  gum  tissue  overlying  pus;  later  it 
softens  at  its  highest  point,  pus  appears  as  a  yellow  spot  beneath  the 
mucous  membrane.  The  mucous  membrane  bursts  and  a  discharge  of 
pus  follows.  The  inflammation  and  tenderness  then  largely  subside, 
but  some  degree  of  looseness  and  protrusion  remains. 

During  the  latter  part  of  the  second  and  in  the  third  stage  of  pus 
formation,  instead  of  the  swelling  extending  but  little  beyond  the 
overlying  gum,  the  tissues  of  the  lips,  cheeks,  or  neck  may  be  very 
much  swollen  and  with  upper  teeth  the  eye  of  the  affected  side  injected. 
In  some  cases  the  outer  skin  may  become  reddened  and  dusky,  ex- 
hibiting the  evidences  of  extension  of  the  inflammatory  process  far 
from  its  original  site. 

While  in  the  vast  majority  of  cases  the  direction  taken  by  the  pus, 
and  the  point  at  which  it  finds  exit,  is  the  buccal  or  labial  aspect,  and 
immediately  over  the  root  apex  of  the  affected  tooth,  or  near  it,  these 
being  the  directions  of  least  resistance,  other  anatomical  conditions 
or  histological  peculiarities  (see  Chapter  VII.)  may  make  the  direc- 
tion of  least  resistance  in  some  other  path  (Figs.  420-423). 

Instead  of  the  circumscribed  suppuration  described  as  the  ordinary 
course  of  abscess  formation  about  the  apices  of  roots  (septic  apical 
pericementitis)  which  accompanies  infection  by  the  staphylococci,  clin- 
ical evidences  of  infection  by  streptococci  occasionally  appear.  The 
inflammatory  process,  instead  of  being  circumscribed,  is  diffuse;  the 
inflammation  extends  along  the  lines  of  the  connective  tissues  and  of  the 
lymphatics;  the  connective  tissues  are  swollen,  the  swelling  extending 
to  the  tissues  of  the  cheek,  down  the  neck,  and  even  to  the  shoulder — 
a  phlegmonous  inflammation.  Instead  of  the  comparatively  free  flow 
of  pus  which  follows  incision  of  the  swelling  in  ordinary  abscess,  pus 
formation  in  streptococcus  infection  is  seen,  upon  incision,  to  be 
limited  and  seropurulent.  While  in  alveolar  abscess  of  the  ordinary 
types  evidences  of  septic  intoxication  or  poisoning  are  unusual,  the 
lymphatics  being  blocked,  as  a  rule,  by  the  inflammatory  exudation, 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  465 

septic  intoxication  and  poisoning  are  the  rule  in  the  erysipelatous 
cases,  those  probably  due  to  streptococcus  infection;  bacterial  poisons 
being  taken  up  by  the  lymphatics  find  their  way  into  the  circu- 
lation. 

The  symptoms  of  the  absorption  of  bacterial  products  from  the 
circumscribed  abscesses  are:  fever,  often  ushered  in  by  a  distinct 
chill.  The  pulse  increases  in  volume  and  tension;  it  is  full,  hard, 
and  frequent.  The  tongue  is  coated,  the  bowels  constipated.  The 
patient  is  also  weakened  and  made  irritable  by  pain  and  attendant 
loss  of  sleep  and  appetite. 

In  the  streptococcal  infection  there  is  danger  that  these  may  change 
into  the  more  profound  symptoms  of  septicaemia — i.  e.,  a  soft,  frequent 
pulse,  repeated  chills,  diarrhoea,  clammy  skin,  general  depression,  and 
a  disordered  nervous  system. 

In  multirooted  teeth  the  inflammation  and  abscess  frequently  appear 
on  only  one  root.  If  the  case  be  seen  early,  before  the  active  exudatiom 
period  of  the  inflammation  sets  in,  the  symptoms  may  be  clearly- 
localized  in  one  root,  the  tooth  exhibiting  tenderness  upon  pressure 
over  the  affected  root,  but  not  upon  the  opposite  side. 

After  spontaneous  discharge  of  the  pus  from  an  abscess,  the  con- 
dition remaining  is  that  of  an  ulcerous  surface  (the  abscess  boundaries),- 
which  is  being  continuously  infected  from  the  putrescent  pulp  rem-- 
nants.  The  conditions,  it  is  seen,  are  not  like  those  of  ordinary  abscess,, 
where  the  infective  material  is  largely  discharged  in  the  pus  evacuation, 
and  the  cells  bounding  the  abscess  wall  dispose  of  remaining  bacteria, 
so  that  regeneration  of  tissue  occurs.  Spontaneous  healing  of  an 
alveolar  abscess  is  the  exception;  the  embryonic  tissue  lining  the 
abscess  walls  being  continuously  infected,  degenerates  and  dies  as  fast 
as  it  forms,  leaving  a  condition  known  as  chronic  alveolar  abscess,  or 
chronic  purulent,  apical,  septic  pericementitis. 

Clinical  History.  The  clinical  history  of  acute  alveolar  abscess  may 
be  divided  into  three  stages:  first,  that  of  initial  inflammation  and 
pus  formation;  secondly,  the  destruction  of  the  alveolar  process; 
thirdly,  the  passage  of  pus  through  the  periosteum  and  mucous  mem- 
brane. The  second  stage  is  usually  the  longest.  The  duration  of 
the  disease  depends  upon  the  readiness  with  which  the  tissues  between, 
the  point  of  beginning  pus  formation  and  its  exit  yield.  When  the 
pulp  chamber  is  open  pus  may  find  exit  by  this  path,  constituting  the 
condition  known  as  blind  abscess — a  misnomer,  because  a  blind 
abscess  is  one  without  a  point  of  discharge,  without  a  fistula  leading. 

30 


466 


DISEASES  OF  THE  PERICEMENTUM. 


to  it;  in  the  cases  discharging  via  the  canal,  the  latter  may  be  con- 
sidered a  fistula  (Fig.  418). 

Acute  abscesses  usually  run  a  short  course,  the  inflammatory  symp- 
toms rarely  being  severe,  and  the  tissue  destruction  limited  (Fig.  418). 
Notably  upon  lower  molars,  and  upon  the  palatal  roots  of  upper 
molars,  the  density  and  thickness  of  bone  overlying  the  roots  may 
make  paths  of  greatly  increased  resistance,  so  that  the  destruction  of 
tissue  proceeds  along  the  line  of  the  pericementum,  the  pus  finding 
exit  at  the  neck  of  the  tooth.  It  is  rare  in  cases  of  lower  second 
molars  and  still  more  rare  upon  the  third  molars,  that  pus  finds 
exit  over  the  apex  of  the  root,  the  dense  bone  of  the  external  oblique 
line  offering  the  greatest  resistance  (Fig.  420).  Over  any  teeth 
the    outer   fibrous   layers  of    the   external   periosteum    may  present 


Fig.  420. 


Fig.  420. — Abscess  uijon  lower  third  molar,  showing  the  usual  paths  of  pus  exit,  A  and  B. 
Fig.  421. — Abscess  upon  palatal  root  of  an  upper  molar  discharging  at  the  neck  of  the  tooth; 

unusual  resistance  to  the  perforative  advance  of  pus,  so  that  when 
the  fibres  of  attachment  of  the  periosteum  have  been  softened  by  the 
inflammation,  and  pus  gains  entrance  between  bone  and  periosteum, 
it  may  travel  or  burrow  along  the  course  of  this  membrane  (Fig.  420), 
depriving  the  bone  of  its  main  nutritive  source,  so  that  limited  necrosis 
threatens.  The  roots  of  the  central  incisors  may  lie  unusually  close 
to  the  floor  of  the  nose,  and  be  overlaid  externally  by  an  unusually 
resistant  layer  of  bone;  in  these  cases  the  path  of  least  resistance  may 
be  in  the  direction  of  the  floor  of  the  nose,  the  abscess  opening  at  that 
point  (Fig.  422),  or  the  pus  may  perforate  the  lingual  alveolar  plate 
and,  raising  the  periosteum  and  mucous  membrane,  form  a  large 
swelling  upon  one  side  of  the  hard  palate  (Fig.  431). 

The  root  apices  of  the  posterior  upper  teeth,  particularly  of  the  first 
and  second  molars,  may  after  the  age  of  twenty-five  or  thirty  be 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS. 


467 


encroached  upon  by  the  enlarging  maxillary  sinus,  so  that  any  or  all 
of  the  roots  of  these  teeth  may  be  separated  from  the  floor  of  the  sinus 
by  but  a  very  thin  lamina  of  bone;  should  abscess  arise  upon  any  of 
these  roots,  pus  discharge  into  the  antrum  would  necessarily  follow. 
In  these  cases  the  acute  symptoms  may  rapidly  subside,  but  later 
symptoms  of  antral  empyema  may  follow  (Fig.  423). 

Resort  to  the  use  of  poultices  upon  the  face,  for  the  relief  of  the  pain 
of  abscess  formation,  may  induce  such  a  softening  of  the  tissues  over 
which  they  are  applied  that  the  passage  of  pus  is  invited  toward  the 
exterior;  the  abscess  may  thus  open  upon  the  face  or  neck,  producing 
permanent,  disfiguring  scars  (Fig.  447). 

In  patients  who  are  in  a  cachectic  condition,  who  have  an  evil 
heredity,  or  whose  tissue  resistance  is  markedly  lessened  in  consequence 


Fig.  422. — Alveolar  abscess  at  the  root  of  a  superior  incisor,  discharging  into  the  nose:  a, 
large  abscess  cavity  in  the  bone;  6,  mouth  of  fistula  on  the  floor  of  nostril ;  c,  lip  ;  d,  tooth. 
(Black.) 

Fig.  423. — Alveolar  abscess  at  the  root  of  an  upper  molar  discharging  into  the  antrum  of 
Highmore :  a,  abscess  cavity  in  the  bone  ;  6,  mouth  of  fistufti  on  the  floor  of  the  antrum  ;  c,  pus 
in  the  antral  cavitj'.     (Black.) 

of  tuberculosis,  or  more  frequently  of  syphilis,  septic  pericementitis 
may  run  a  riotous  course;  the  bone  suffers  extensively  by  direct  action; 
the  periosteum  is  undermined,  is  stripped  from  the  bone  over  large 
areas,  and  breaks  down  readily;  so  that  while  in  the  healthy  person 
alveolar  abscess  formation  may  run  a  direct  course  and  find  prompt 
outlet,  in  the  syphilitic  patient  extensive  pus  infiltration,  with  necrosis, 
may  occur.  In  cachectic  persons  lymphatic  involvement  is  common; 
waste  products  of  bacterial  origin,  find  their  way  into  the  lymphatics, 
and  set  up  secondary  irritative  processes  in  the  nearest  lymphatic 
glands — lymphadenitis . 

In  persons  whose  oral  hygiene  is  neglected  the  third  stage  of  alveolar 


468  DISEASES  OF  THE  PERICEMENTUM. 

abscess   is   frequently  violent   and    the    inflammatory  process  wide- 
spread. 

Diagnosis.  In  incipient  apical  pericementitis  the  symptoms  may 
consist  of  reflex  pains,  but,  as  a  rule,  are  distinctly  localized  in  the 
teeth  affected,  which  are  tender  to  the  touch.  The  discoloration  of 
the  tooth  crown  and  other  evidences  of  moist  gangrene  are  usually 
present  unless  the  tooth  has  been  previously  partially  treated,  when 
the  color  may  be  good,  but  by  transmitted  light  opacity  is  noted. 
In  the  pronounced  cases  the  symptoms  are  as  described. 

After  high  inflammation  has  existed  for  twenty-four  hours,  pus  is 
generally  present  in  the  apical  tissue  (Fig.  424). 

Of  two  pulpless  teeth  surrounded  by  a  zone  of  inflammation  the 
most  tender  is  the  one  affected,  though  both  may  be  acting  at  once. 

It    is  to  be    remembered    that    adjoining, 
^^^'  ^"^'  otherwise    normal,  teeth    may  show    some 

evidence  of  pericementitis,  so  that  differen- 
tiation is  necessary.  The  various  stages  of 
inflammation  and  pus  formation  are  judged 
by  the  appearance  of  the  gum  or  by  the 
•T-ray  Fig.  424.  The  greater  the  swelling 
and  injection  of  the  gum,  the  more  ad- 
vanced is  the  pus  formation. 

The    inflammatory   action    precedes    the 
advance  of  pus,  which  furnishes  a  guide  to 


Diagnosis  of  apical  abscess  by        ,  , .  .  , 

a;-rays.     (Price.i)  the     dirCCtlOn      the     pUS     IS      purSUmg VIZ., 

where  the  most  intense  coloration  and  the 
greatest  swelling  appear  will  be  the  point  at  which  the  abscess  will 
point  or  discharge.  A  sudden  subsidence  of  inflammation  without  an 
immediately  discoverable  point  of  pus  exit  should  lead  to  the  suspicion 
that  the  discharge  has  taken  place  in  an  unusual  situation. 

An  abscess  originating  about  an  impacted  tooth,  or  one  due  to 
subperiosteal  inflammation,  must  be  differentiated.^ 

A  pericemental  abscess  must  also  be  considered.  An  acute  abscess 
of  the  pulp  in  its  most  pronounced  stage  may  simulate  incipient  or  even 
pronounced  acute  apical  pericementitis.     (See  p.  407.) 

The  last  three  conditions  are  usually  associated  with  suspected 
teeth  containing  vital  pulps,  so  that  tests  for  pulp  vitality  are  to  be 
applied. 

In  certain  cases  of  pulp  gangrene  part  of  the  pulp  only  may  be 

1  Items  of  Interest,  1901.  2  Black,  American  System  of  Dentistry,  vol.  i. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  469 

dead — e.  g.,  the  lingual  filament  of  the  pulp  of  an  upper  molar;  while 
the  balance  may  be  vital  (the  buccal  filaments) .  This  fact  may  confuse 
the  response  to  tests  and  is  to  be  borne  in  mind. 

Prognosis.  In  the  majority  of  cases  the  prognosis  of  acute  alveolar 
abscess,  as  to  the  future  retention  of  the  tooth,  is  favorable;  and  usually 
very  favorable,  if  the  case  receive  intelligent  therapeutic  aid.  The 
future  of  the  tooth  depends  upon  the  thoroughness  with  which  sources 
of  infection  may  be  destroyed  and  permanently  removed,  and  the 
completeness  with  which  regeneration  of  tissue  can  be  induced. 

Treatment.  In  the  initial  inflammation  and  first  stage  of  pus 
formation  the  treatment  should  be  abortive.  The  cause  of  the  inflam- 
mation should  be  removed,  if  possible,  and  the  pus  formed  be  removed 
or  at  least  permitted  to  escape  by  way  of  the  pulp  canals.  The  prompt- 
ness of  relief  from  pain  depends  upon  the  thoroughness  with  which 
this  is  accomplished. 

The  pulp  chamber  should  be  opened  to  an  extent  which  permits 
the  free  passage  of  broaches  into  the  canal  (Figs.  418  and  421). 

If  the  cavity  of  decay  be  open  the  pulpal  wall  is  to  be  perforated. 
If  a  filling  be  present,  it  is  in  part  or  entirely  removed.  If  the  enamel 
be  entirely  sound,  or  if  subsequent  treatment  require  a  new  opening 
in  line  with  the  pulp  canals,  it  is  at  least  in  part  made. 

These  openings  are  usually  begun  with  a  small,  spear-pointed  drill 
(No.  101  S.  S.  W.  Catalog)  revolving  in  a  perfectly  true  hand-piece. 
The  opening  made  is  enlarged  with  successive  sizes  of  sharp,  round, 
dentate  burs  until  of  sufficient  size. 

According  to  the  amount  of  tenderness,  the  tooth  will  require  a 
counterpressure  to  that  of  the  drill.  If  the  entrance  be  made  through 
the  occlusal  face  of  the  tooth,  or  in  a  direction  which  would  cause 
direct  pressure  on  the  apical  pericementum,  a  ligature  of  linen 
thread  with  long  ends  may  be  placed  around  the  tooth,  and  traction 
be  made  by  drawing  on  the  loose  ends  of  the  ligature.^  Effective 
counterpressure  against  lateral  entrance  to  the  pulp  chamber  may 
be  made  by  softening  a  small  roll  of  modelling  compound  and  mould- 
ing over  the  face  of  the  affected  tooth  and  several  of  those  adjoining 
it,  and  permitting  it  to  harden.  This  temporary  splint  is  held  in 
place  by  the  index  finger  of  the  left  hand.  In  case  the  inflammatory 
process  is  marked,  it  may  be  necessary  to  make  a  vent  opening  by 
the  most  direct  path — i.  e.,  at  the  junction  of  enamel  and  cementum 
— directly  into  the  chamber. 

'  J.  Foster  Flagg,  Lectures  on  Dental  Therapeutics. 


470  DISEASES  OF  THE  PERICEMENTUM. 

As  soon  as  entrance  to  the  pulp  chamber  is  effected,  the  cavity  is 
syringed  with  a  strong  antiseptic;  a  20  per  cent,  sokition  of  meditrina 
answers  well  in  this  connection.  Fine  probes  are  passed  and  repassed 
into  the  opening  to  free  the  outlet,  so  that  gases  may  escape  and  fresh 
portions  of  the  antiseptic  be  worked  into  the  cavity.  The  cjuickness 
with  which  relief  is  secured  will  depend  upon  the  thoroughness  with 
which  the  canals  are  entered  and  their  putrid  contents  destroyed.  A 
tedious  class  of  cases  are  those  in  which  a  canal  of  a  molar  is  unfilled 
or  but  partially  filled.  Unless  entrance  to  and  cleansing  of  the  canal 
be  accomplished,  the  inflammation  will  proceed  until  the  pus  finds 
external  vent.  An  hour  spent  in  gaining  access  to  and  cleansing  such 
canals  is  well  spent. 

If  entrance  to  the  canals  be  free,  repeated  applications  of  sodium 
dioxide  solutions  should  be  made,  pumped  into  the  canals,  and  the 
cavity  washed  from  time  to  time  with  meditrina  or  hydrogen  dioxide. 
Near  the  end  of  the  canal  the  meditrina  is  used  alone  with  broaches, 
and  finally  by  syringing.  The  canals  are  dried,  and  an  anodyne  anti- 
septic, such  as  phenol-camphor  plus  menthol,  is  pumped  into  the  canals. 
If  now  provision  for  surgical  rest  of  the  irritated  pericementum  be 
made,  relief  is  tolerably  certain. 

A  moldine  impression  may  be  taken  of  a  tooth  at  some  distance; 
from  this  a  fusible  metal  die  is  made,  which  is  driven  into  soft  lead 
for  a  counter-die.  Between  these  is  swaged  a  metal  cap  (German  silver, 
26  gauge,  will  do),  to  cover  the  occlusal  and  part  of  the  buccal  and 
lingual  surface.  This  is  attached  to  the  dried  tooth  by  means  of  zinc 
phosphate  and  allowed  to  remain  a  day  or  two.  As  a  quickly  made 
substitute,  a  strip  of  rubber-dam  about  three  inches  long  and  about 
seven-eighths  inch  wide  is  rolled  into  a  pad  of  the  width  of  the  occlusal 
face  of  the  tooth  to  be  capped.  Floss  silk  is  then  sewed  through  this 
in  such  a  manner  as  to  cause  it  to  tie  the  pad  over  the  tooth,  the  silk 
itself  encircling  the  neck  of  the  tooth. ^  This  will  ensure  rest  of  the 
affected  pericementum  (Fig.  425). 

A  mixture  of  tincture  of  aconite  and  tincture  of  iodine  or  dental 
tincture  of  aconite  should  be  then  painted  upon  the  gum  over  the 
topth.^  The  inflammation  usually  subsides  and  almost  disappears  in 
a  couple  of  days.  The  local  measures  should  be  supplemented  in 
somewhat  severe  cases  by  the  administration  of  a  saline  cathartic  or 

1  Flagg. 

-  Dental  tincture  of  aconite  may  be  made  by  evaporating  the  oflBcial  tincture  to  one-fourth  its 
bulk.  It  should  be  used  with  great  care,  and  be  covered  for  a  half-hour  with  a  pad  of  cottonoid. 
The  patient  should  be  cautioned  against  swallowing  the  saliva  during  this  time.    (Flagg.) 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  471 

the  hot  pedikivium  as  derivatives.  Instead  of  catharsis  the  hot  pedi- 
luvium  and  diaphoresis  may  be  conjoined;  10  grains  of  Dover's 
powders  in  hot  lemonade  are  to  be  taken  after  the  pediluvium^  and 
the  patient  well  covered  up  in  bed.  These  several  measures  are  to  be 
regarded  as  the  abortive  treatment  of  alveolar  abscess;  they  apply  to 
all  cases  if  seen  early  enough,  and  will  in  the  majority  of  cases  prevent 
the  disease  of  the  pericementum  passing  the  early  inflammatory  stages. 
In  all  cases  the  severity  of  the  inflammatory  process  is  lessened  in 
proportion  to  the  thoroughness  with  which  the  antiseptic  measures 
are  applied,  provided  that  in  the  attempt  at  such  application  no  septic 
matter  be  violently  thrust  through  the  apical  foramen. 

While  this  is  true,  marked  relief  is  so  often  given  in  even  severe  cases 
by  the  simple  opening  of  the  pulp  chamber  by  means  of  a  spear  drill, 
thus  permitting  the  gases  and  pus  to  find  vent,  that  in  those  cases  in 
which  tenderness  of  the  tooth  prevents  thorough  opening,  or  when 
patients  are  confined  to  bed  by  illness,  such  an  opening  may  be  made, 
either  at  the  neck  of  the  tooth  or  through  a  filling. 


Rubber-dam  guard  for  use  in  pericementitis:  A,  roll  of  dam  threaded;  B,  guard  fitted  over 
tooth ;  tooth  eliminated  to  show  the  manner  in  which  the  silk  encircles  it. 

In  the  second  stage  of  pus  formation  the  abortive  treatment  may 
still  be  attempted.  In  some  cases  this  is  successful  in  at  least  reducing 
the  acute  pain  which  demoralizes  the  patient. 

If  the  pain  persist,  the  gum  and  bone  overlying  the  apical  space 
should  be  perforated  in  order  to  form  an  artificial  fistula. 

Black's  method  is  a  good  one.  A  few  drops  of  carbolic  acid  are 
placed  on  a  glass  slab  and  a  deeply  serrated  plugger  point  is  dipped 
into  this,  and  the  tiny  drop  adherent  is  laid  upon  the  gum,  which  it 
eschars  and,  in  part,  anaesthetizes.  The  serrated  point  is  used  to 
scratch  theescharred  tissue;  more  carbolic  acid  is  added  and  the  pro- 
cess repeated  until  the  bone  is  reached.  A  fresh  drop  is  then  placed 
and  the  bone  perforated  with  a  sharp  chisel  or  a  spear  drill.     The 

1  Endelman  (Dental  Cosmos,  March,  1904)  suggests  the  rational  improvement  of  immersing 
the  feet  in  warm  water  which  is  gradually  made  hotter,  as  bearable,  until  the  vessels  of  the 
feet  become  well  engorged. 


472 


DISEASES  OF  THE  PERICEMENTUM. 


KiG.  426. 

C    o    o 


;ijy 

m 

4      6     5 

Tubular  knives. 


location  of  the  ab.scess  may  be  determined  by  measuring  the  length 
of  the  root  by  the  use  of  a  Donaldson  hook,  over  the  shank  of  which 
a  disk  of  rubber-dam  has  been  passed  as  a  guide. 

The  ffum  mav  be  refrigerated  with  ethyl  chloride  or  a  little  cocaine 
solution  may  be   injected  into  it  and  a  deep    cut  be   made  to  the 

bone,  after  which  the  perforation  of 
the  bone  is  made.  After  cocainizing 
the  parts  a  Rollins  tubular  knife 
may  be  used  to  remove  a  circular 
section  of  gum  tissue,  after  which  a 
fine  trephine  or  the  drill  may  be 
employed  to  enter  the  apical  space. 
The  difficulty  of'  determining  the 
exact  location  of  the  abscess  seat 
renders  this  operation  of  perforation 
almost  impracticable  in  some  cases. 
Under  such  circumstances  the  abor- 
tive treatment,  both  local  and  sys- 
temic, must  be  made  as  thorough 
as  possible,  and  if  not  successful  the  patient  may  be  kept  under  the 
influence  of  morphine  until  such  time  as  the  pus  formation  has  reached 
the  third  stage.  This  may  be  hastened  by  the  use  of  a  capsicum 
plaster  applied  to  the  gum.  This  may  properly  be  denominated  the 
expectant  treatment,  and,  while  perhaps  unsurgical,  presents  at  times 
no  alternative  but  tooth  extraction. 

As  a  preventive  of  possible  blood  infection  the  following  may  be 
administered: 

]^ — Hydrargyri  hichloridi,  gr.  j. 

Tinct.  ferri  chloridi,  fSj. — M. 

Sig. — Twenty  drops  in  water  four  times  a  daJ^ 

In  case  the  patient  suffer  marked  physical  debility  owing  to  pain 
and  intestinal  disturbance,  a  stimulant  tonic  should  be  used  after  the 
use  of  the  saline  cathartic. 


Walker- Younger 
trephines. 


{fc— Saloli, 

Quininse  sulphatis,  da    gr.  xxx. 

M.  et  fiant  capsulse  No.  x. 
Sig.— Take  one  capsule  before  each  meal  and  on  retiring. 

This  combination  acts  as  tonic,  antipyretic,  and  antiseptic. 
The  following^  is  also  suggested  as  analogous: 


1  Endelman,  Dental  Cosmos,  1904. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  473 


It— Quininee  sulphatis, 

gr.  XXX. 

Acetanilid, 

gr.  xxiv 

CaffeinEe  citratis, 

gi--  iij. 

M.  et  fiant  pil.  No.  xij. 

Sig.— One  every  hour. 

In  the  third  stage  the  pus  is  in  the  tissues  exterior  to  the  alveolar 
process.  A  deep,  free  incision  should  be  made  in  order  to  evacuate 
the  abscess ;  a  methyl  chloride  spray  or  a  cocaine  injection  being  used 
as  an  anaesthetic  in  those  cases  in  which  the  pus  is  deep  seated. 

The  abscess  cavity  is  then  to  be  syringed  out  with  hamamelis 
(distillate)  and  afterward  with  hydrogen  dioxide. 

It  has  been  recommended  that  at  this  time  the  root  end  be  scraped 
or  amputated  as  a  means  of  ensuring  the  cure  of  the  abscess.  There 
can  be  no  objection  to  the  removal  of  shreds  of  necrotic  tissue  about 
the  root  apex,  nor  even  to  slight  amputation  if  the  operation  be 
endurable.  The  great  majority  of  these  cases  are,  however,  curable 
by  correct  root-canal  treatment,  and  the  inflammatory  symptoms  and 
conditions  under  which  one  operates  seem  to  indicate  that  a  better 
course  is  to  introduce  a  drain  of  antiseptic  gauze  into  the  abscess 
cavity  through  the  incision  in  order  that  the  fistula  shall  not  close 
externally.     Upon  the  cheek  should  be  placed  compresses  wet  with 


antiphlogistic. 

It — Liquor  plumbi  subacetatis, 

f3iv. 

Tinct.  opii, 

Sj. 

Aquas, 

oj.- 

The  root  canals  need  not  necessarily  be  opened  at  this  time.  In  a 
day  or  two  the  intense  inflammatory  symptoms  should  have  subsided. 
If,  later,  the  treatment  for  chronic  abscess  be  not  successful,  the 
abscess  cavity  may  be  packed  open  with  antiseptic  gauze  and  the  root 
end  amputated  under  conditions  vastly  more  favorable  to  success. 
(See  Treatment  for  Chronic  Apical  Abscess.) 

Under  no  circumstances  should  hot  poultices  be  applied  to  the  out- 
side of  the  face,  as  a  discharge  of  pus  in  that  direction  will  cause  a  dis- 
figuring scar.  If  an  abscess  threaten  to  open  externally  the  abscess 
should  be  opened  by  an  incision  made  from  a  point  within  the  mouth, 
and,  after  sterilization  of  the  tract,  a  drainage  tent  of  antiseptic  gauze 
should  be  introduced  nearly  to  the  bottom  of  the  pus  cavity.  This 
should  be  removed  daily,  the  abscess  cavity  sterilized,  and  the  tent 
renewed.  An  antiphlogistic  compress  should  be  applied  to  the  face. 
The  principal  object  sought  is  the  mechanical  apposition  of  the 
walls  of  the  abscess  cavity  at  the  dependent  or  external  portion,  in 
order  that  these  shall  unite  by  granulation  and  that  the  fistula  shall 


474  DISEASES  OF  THE  PERICEMEXTUM. 

in  this  manner  become  an  ordinary  one.     The  patient  should  he  in 
a  position  to  counteract  the  natural  effect  of  gravitation. 

After  lancing,  the  mouth  should  be  kept  well  sterilized  by  frequent 
sprays  or  gargles  of  hydrogen  dioxide,  which  may  be  diluted  to  one- 
third  strength  with  water — /.  e.,  to  a  1  per  cent,  solution. 

If,  in  connection  with  the  lower  third  molar,  marked  swelling  be 
observed  in  the  submaxillary  triangle,  free  incision  of  the  tissues  of 
the  floor  of  the  mouth  should  be  made  at  the  angle  of  junction  with 
the  bone.  The  cut  should  be  made  close  to  the  bone  and  toward  it, 
but  not  too  deep,  lest  the  mylohyoid  artery  or  nerve  be  injured. 

The  deep  lancing  of  an  abscess  upon  the  hard  palate  may  cause 
a  cut  to  be  made  in  the  posterior  palatine  artery.  External  to  the 
lower  jaw  the  facial  artery  is  to  be  considered. 

It  is  ever  to  be  borne  in  mind  that  so  long  as  the  source  of  infection 
remains  pus  formation  continues,  and  so  long  as  pus  forms  tissue 
destruction  is  in  progress;  furthermore,  in  proportion  to  the  amount 
of  tissue  loss  perfect  recovery  after  alveolar  abscess  is  delayed  or 
imperfect. 

^^  hile  it  is  the  clinical  experience  of  nearly  every  operator  that  a 
tooth  and  adjacent  structures  may  recover  from  inflammation  which 
involves  not  only  the  first  tooth  attacked,  but  by  an  extension  of  the 
inflammatory  process  involves  the  general  periosteum  and  neighboring 
teeth,  provided  the  case  receive  prompt  and  decisive  surgical  treatment, 
yet  the  danger  of  necrosis  and  septicaemia  in  prolonged  cases  is  always 
imminent.  When  the  general  periosteum  is  involved,  as  shown  by 
extensive  boggy  swelling  in  the  mouth,  if  several  free  incisions  carried 
to  the  bone  do  not  afford  prompt  relief,  the  tooth  which  is  the  centre 
of  infection  should  be  promptly  extracted.  If,  in  the  continued  course 
of  the  pericementitis,  chills,  followed  by  fever,  a  coated  tongue,  and 
much  physical  depression  occur,  a  general  infection  is  to  be  feared, 
and  no  time  should  b0  lost  in  sterilizing  the  mouth,  extracting  the 
tooth,  and  subjecting  the  socket  to  free  spraying  with  antiseptics. 

It  has  been  a  subject  of  controversy  whether  a  tooth  should  be 
extracted  while  the  abscess  is  forming.  It  has  been  claimed  that  the 
continuation  of  pus  formation  after  extraction  renders  the  state  of  the 
patient  even  worse  than  before  extraction. 

This  occurrence  is  comparatively  infrequently  seen,  and  is,  of  course, 
due  either  to  the  retention  of  some  pyogenic  organisms  beneath  the 
clot  which  forms  in  the  alveolus  or  the  infection  of  the  parts  by  ex- 
traneous organisms. 


ACUTE  SEPTIC  APICAL  PERICEMENTITIS.  475 

The  retention  of  the  tooth  until  a  fistula  forms  would  also  confine 
the  bacteria  for  the  time. 

In  cases  of  extraction  during  the  second  stage  of  pus  formation,  the 
alveolus  should  be  forcibly  syringed  for  ten  minutes  with  hydrogen 
dioxide,  in  every  four  ounces  of  which  two  grains  of  mercuric  chloride 
has  been  dissolved.  If  thought  desirable  to  repeat  the  syringing,  a  tent 
of  antiseptic  gauze  may  be  gently  carried  to  the  apex  of  the  alveolus 
and  left.  This  tent  may  be  removed  to  permit  syringing,  and  should 
never  be  left  long  at  any  one  time,  as  septic  inflammation  of  the  alveolar 
walls  may  occur. 

In  cases  of  this  kind  oral  sterilization  and  derivative  systemic  medi- 
cation are  of  importance.  As  soon  as  improvement  is  noted  the  tent 
should  be  removed,  the  alveolus  sterilized  as  before,  and  a  new  clot 
induced  by  a  curetting  of  the  walls.  The  case  should  now  proceed 
as  any  ordinary  extraction. 

In  cachectic  individuals  acute  abscesses  may  cause  inflammation 
of  the  deeper  tissues  and  of  the  periosteum  as  well,  and  extensive 
necrosis  may  occur. 

Acute  septic  apical  pericementitis  may  occur  on  a  temporary  tooth, 
most  frequently  a  temporary  molar.  The  symptoms  and  pathology 
are  the  same,  except  that  the  looser  character  of  the  alveolar  structure 
seems  to  frequently  permit  the  abscess  to  assume  the  chronic  form 
before  the  dentist  is  consulted.  Children  often  hide  these  conditions 
from  their  elders  out  of  fear  of  the  dentist.  In  strumous  children  the 
inflammation  may  be  spreading  and  the  lymphatic  glands  may  be 
involved.  There  may  also  be  some  symptoms  of  septic  intoxication 
evidenced  by  chills  accompanied  by  fever,  etc.  These  cases  require 
an  opening  of  the  abscess,  sterilization  of  the  part,  and  attention  to 
the  systemic  condition.  If  seen  in  the  acute  stage  the  treatment  is 
the  same  as  for  the  permanent  teeth,  unless  the  disease  occur  shortly 
before  the  date  for  eruption  of  the  permanent  successor,  when  the 
temporary  tooth  should  be  extracted.  If  treated,  the  canals  should 
be  filled  with  materials  which  can  be  resorbed  by  the  tissues,  such 
as  parafiin  or  wax  with  aristol. 


CHAPTER     XXI. 

CHRONIC  SEPTIC,  PURULENT,  APICAL  PERICEMENTITIS 
(CHRONIC  APICAL  ABSCESS). 

By  this  title  is  meant  a  condition  of  apical  pericementitis  due  to 
septic  influences  in  which  pus  is  continuously  formed  at  the  expense 
of  the  apical  pericementum  and  contiguous  tissues.  It  is  the  usual 
outcome  of  acute  apical  abscess,  and  is  established  as  soon  as  the 
pus  finds  vent  either  through  the  gum  as  a  natural  result  or  through 
the  root  canal  as  the  result  of  surgical  interference  or  the  opening  of 
the  canal  by  caries. 

These  two  avenues  of  pus  escape  give  the  two  clinical  conditions  of 
(1)  chronic  apical  abscess  discharging  via  the  root  canal;  (2)  chronic 
apical  abscess  with  fistula. 

CHRONIC  APICAL  ABSCESS  DISCHARGING  VIA  THE 
ROOT  CANAL. 

Pathology  and  Morbid  Anatomy.  First  Grade.  Upon  abortion  of 
an  acute  abscess  in  the  first  stage  the  pressure  of  pus  upon  the  apical 
tissues  is  released  and,  as  a  rule,  the  walls  of  the  abscess  cavity  throw 
out  granulations  which  fill  it.  This  tissue  tends  to  organize  into  more 
or  less  healthy  tissue  (cicatricial  tissue).  The  bacteria  are  killed  out 
except  at  that  part  represented  by  immediate  contact  with  the  root 
foramen ;  at  this  point  the  tissues  are  infected  and  some  molecular  loss 
of  tissue  as  pus  may  occur.  A  limited  loss  of  granulation  tissue  by 
pus  formation  is  compensated  for  by  the  formation  of  new  granu- 
lations. The  conditions  are  almost  analogous  to  those  existing  in 
moist  gangrene  of  the  pulp  and  require  analogous  treatment. 

Second  Grade.  If  the  abortion  of  the  abscess  have  only  partly 
permitted  the  pus  to  drain,  or  the  alveolar  walls  or  crypts  of  the  abscess 
wall  remain  infected,  the  pus  will  continue  to  form  and  escape  in 
some  degree  via  the  canal.  If  the  tooth  now  be  extracted  a  small  abscess 
sac  will  be  found  upon  the  root  end.  If  opened  this  will  be  seen  to 
be  a  mass  of  fibrous  vascular  tissue  (inflamed  pericemental  apical 
tissue)  having  a  central  lumen  connecting  with  the  root  canal  (the 
abscess  cavity). 


CHRONIC  APICAL  ABSCESS.  477 

Third  Grade.  With  partial  vent  to  the  pus  formed,  the  abscess 
cavity  of  the  second  grade  may  enlarge,  involve  the  bony  walls  of 
the  alveolus,  and  the  soft  tissues  then  proliferate  to  such  an  extent  that 
they  finally  organize  into  a  large,  fibrous,  vascular  sac  attached  to  the 
tooth.  This  sac  has  the  central  pus  cavity  be- 
fore described,  which  is  connected  with  the  pulp 
canal.  It  may  be  a  half-inch  or  more  in  length 
(Fig,  428)  and  may  be  extracted  with  the  tooth 
or  may  be  left  attached  to  the  bone.  It  neces- 
sarily occupies  in  the  latter  a  cavity  of  a  size 
corresponding  to  its  own  bulk.  As  its  inner 
walls  are  infected,  extraction  without  its  removal 
leaves  an  infected  area  which  must  be  disinfected       chronic  apical  abscess, 

,  ,  ,  third  grade :  B,  abscess  sac 

or  a  secondary  acute  abscess  may  result.  containing  a  central  pus 

Fourth  Grade.     Instead  of   organizing  the    cavity;  d.  apex  of  root; 

"  '-'  C,  canal  containing  pus. 

fibrovascular  tissue  may  be  liquefied  into  pus. 
The  root  apex  becomes  denuded  for  a  distance  about  the  apical 
foramen.  Pus  collects  about  the  apex  of  the  root  and  rests  upon 
the  bone  owing  to  the  influence  of  gravity.  The  bone  is  thus  in- 
fected, inflamed,  and  further  liquefied,  while  necessarily  the  abscess 
cavity  enlarges.  If  a  bistoury  be  thrust  through  the  labial  alveolar 
wall  in  such  a  case  as  shown  in  Fig.  429,  but  slight  resistance  will 
need  to  be  overcome.  In  the  lower  jaw  the  tendency  is  to  burrow 
into  the  cancellated  tissue  of  the  bone  away  from  the  tooth,  so  that 
destruction  of  the  pericementum  may  not  be  very  extensive.  In  the 
upper  jaw  the  tendency  is  to  spread  along  the  pericementum  and  into 
the  cancellated  bone,  so  that  the  cavities  of  chronic  abscess  upon  the 
upper  anterior  teeth  particularly  may  cause  extensive  excavation  in 
the  palatal  process  of  the  superior  maxillary  bone  (Fig.  431).  The 
pus  may  burrow  in  irregular  and  circuitous  directions,  until  it  finds 
external  vent. 

In  long-established  cases  deposits  of  pus  calculi  (serumal)  may 
form  upon  the  root  end  (Fig.  432).  The  cement  corpuscles  of  the 
apical  cementum  may  die  and  the  root  tissue  itself  become  infected. 
In  other  cases  resorption  of  the  root  end  occurs.     (See  Resorption.) 

Symptoms.  In  all  of  these  cases  the  formations  are  gradual  owing 
to  the  partial  vent,  and  it  may  be  that  no  pain  beyond  a  slight  gnaw- 
ing or  feeling  of  fulness  or  an  occasional  reflex  pain  may  occur.  If 
for  any  reason  the  vent  become  occluded,  the  pus  formation  becomes 
rapid  and  an  acute  abscess  is  set  up,  which  may  be  painful  or  not, 


478 


DISEASES  OF  THE  PERICEMEXTUM. 


according  to  the  amount  of  tension  produced  before  discharge  of  the 
pus.  Aside  from  this  the  gum  color  at  the  apex  is  somewhat  deepened, 
the  tooth  is  shghtly  loosened,  and  slightly  tender  to  percussion.  Signs 
of  previous  moist  gangrene  are  in  evidence. 


Fig.  129. 


Fig.  430. 


Chronic  blind  abscess  of  upper  incisor,  showing 
tendency  of  pus  to  progressively  destroy  perice- 
mentum, owing  to  the  influence  of  gravity. 


Chronic  blind  abscess  upon  lower 
tooth,  showing  tendency  of  pus  to  sink 
into  the  substance  of  the  lower  maxilla, 
owing  to  the  influence  of  gravitj'. 


Diagnosis.  The  passage,  without  production  of  sensation,  of  an 
undue  length  of  fine  probe  into  a  canal  is  evidence  of  destruction  of 
apical  tissue  and  a  guide  to  its  probable  extent. 


Chronic  apical  abscess  discharging  through 
the  hard  palate  and  threatening  to  discharge 
labially. 


Chi-onic  abscess,  showing  denudation 
of  apes  of  root  (a  to  6),  with  deposits  of 
calculi  (a)  upon  cementum. 


An  extensively  inflamed  gum  tissue  over  the  apex  indicates  a  prob- 
able approach  of  pus  formation  to  gum  tissue.  The  presence  of  pus 
in  the  canal  or  upon  several  dry  cottons  introduced  for  absorbent 


CHRONIC  APICAL  ABSCESS.  479 

purposes  is  diagnostic.  If  pus  be  not  seen,  and  the  canal  be  thoroughly 
sterilized  and  dressed  with  an  antiseptic,  the  supervention  of  an  acute 
abscess  affords  evidence  of  the  presence  of  an  abscess  sac  or  cavitv. 
The  x-ray  affords  a  means  of  diagnosis  (Fig.  424). 

Prognosis.  The  prognosis  is  favorable  to  a  cure  in  nearly  all  of 
these  cases,  provided  thorough  canal  asepsis  and  filling  can  be  attained 
and  the  abscess  ca\ity  can  be  drained-  and  disinfected.  In  cases 
resisting  this  treatment,  amputation  of  the  root  end  or  replantation 
will  cure  a  certain  percentage  of  cases.  In  all  other  cases  extraction 
should  be  resorted  to. 

Treatment.  The  first  and  second  grades  of  chronic  alveolodental 
abscess  discharging  via  the  canal  may  be  treated  upon  exactly  the 
same  principles  which  are  involved  in  the  treatment  of  moist  gangrene 
of  the  pulp.  The  infection  is  considered  as  simply  more  deep  seated, 
so  that  it  is  necessary  to  pass  disinfectants  into  the  abscess  cavity 
with  two  objects  in  view:  (1)  to  destroy  the  bacteria  present;  (2)  to 
stimulate  the  tissues  to  granulative  activity.  To  accomplish  this  the 
apical  foramen  must  be  opened.  The  canal  should  be  sterilized  with 
sodium  dioxide  and  the  foramen  enlarged  with  a  fine  Donaldson 
cleanser,  the  canal  having  been  flooded  with  meditrina  or  a  10  per 
cent,  solution  of  zinc  chloride  in  water  as  an  antiseptic. 

If  necessary  the  root  canal  may  be  otherwise  enlarged.  (See  p.  432.) 
If  removable  but  otherwise  permanent  antiseptic  root  fillings  be 
introduced  (see  p.  437)  and  counterirritants  be  applied  to  the  gum, 
the  chances  are  that  in  a  great  majority  of  the  cases  any  resultant 
irritation  will  be  of  a  passing  character  and  symptomatic  of  an  aseptic 
inflammation.  In  cases  in  which  the  canal  cannot  be  explored  even 
by  the  aid  of  the  known  means  of  enlargement,  it  is  to  be  assumed 
that  the  end  of  the  root  is  curved  or  the  canal  in  some  unknown  way 
occluded,  and  it  is  well  to  employ  Rhein's  method  of  cataphorically 
producing  zinc  oxychloride  in  situ,  or  Bethel's  nitrate  of  silver 
method  (see  p.  453),  or  25  per  cent,  ethereal  pyrozone  or  formal- 
dehyde solution  (5  to  20  per  cent.)  may  be  introduced  on  cotton  for 
twenty-four  hours.  At  the  end  of  that  time  the  root  canal  is  to  be 
opened  under  aseptic  precautions  and  the  canal  examined  for  the 
presence  of  pus.  No  pus  may  be  noted  upon  the  cotton  dressing,  but 
if  sterilization  has  failed  the  pus  may  later  be  found  upon  cotton 
introduced  as  an  absorbent. 

In  these  cases  these  or  other  dressings  may  be  renewed  every  other 
day  until  pus   formation  ceases;  some  operators  prefer  to  leave  a 


480  DISEASES  OF  THE  PERICEMENTUM. 

small  vent  in  the  temporary  covering,  used  to  act  as  a  drain.  This, 
however,  is  apt  to  prevent  the  concentration  of  the  action  of  the 
medicament  upon  the  apical  tissue. 

After  sterilization  of  the  abscess  sac  and  the  canal,  whether  this  be 
accomplished  immediately  or  by  tentative  dressings,  the  pulp  canal 
may  be  filled  with  a  removable  antiseptic  root  filling  (Forma-Percha, 
aristol  and  wax,  paraform  and  wax,  etc.)  and  a  temporary  cavity 
filling  inserted.  After  a  test  of  a  w^eek  or  two  the  cavity  may  be 
filled. 

If,  on  the  other  hand,  pus  formation  increase  or  be  persistent,  an 
artificial  fistula  must  be  established  (see  p.  471)  and  the  case  treated 
as  a  chronic  apical  abscess  with  fistula. 

In  the  third  and  fourth  grades  the  prognosis  for  treatment  by  way 
of  the  canal  is  not,  as  a  rule,  good.  If,  however,  an  artificial  fistula 
be  established  the  ease  of  treatment  is  greatly  increased.  The  case  is 
then  treated  as  a  chronic  apical  abscess  with  fistula. 

In  no  case  should  hydrogen  dioxide  be  forced  in  quantity  into  the 
pus  occupying  such  an  abscess  cavity  until  the  fistula  has  been  made> 
and  it  is  better  even  then  that  the  bulk  of  it  be  washed  out  with  warm 
water  before  applying  the  drug.  A  neglect  of  this  precaution  may 
bring  about  great  pain,  owing  to  the  rapid  reaction  of  the  hydrogen 
dioxide  with  the  pus  present. 

CHRONIC  APICAL  ABSCESS   WITH  FISTULA. 

Morbid  Anatomy  and  Pathology.  This  form  of  chronic  abscess 
occurs  as  the  result  of  the  discharge  of  an  acute  abscess  through  the 
gum  or  other  part  to  the  surface  of  the  body.  (The  interior  of  the 
mouth  or  other  cavity  exposed  to  contact  with  the  air  is  considered 
external  to  the  l)ody  proper.) 

If  the  acute  abscess  has  been  severe  or  long  continued  the  tissue 
destruction  may  be  great,  but,  as  a  rule,  granulation  promptly  sets 
in  and  the  walls  of  the  abscess  cavity  organize  into  cicatricial  tissue. 
From  the  interior  of  this  a  canal  (fistula)  lined  with  cicatricial  tissue 
leads  to  the  surface,  the  pus  being  almost  constantly  formed  at  the 
expense  of  the  granulation  tissue  which  is  as  constantly  renewed. 

The  fistulous  opening,  as  a  rule,  appears  as  a  small  teat  of  inflamed 
tissue  located  in  the  majority  of  cases  upon  the  buccal  surface  of  the 
gum,  about  a  quarter  of  an  inch  below  the  apex  of  the  root  and  slightly 
distal  to  it— a  position  probably  determined  by  the  density  of  the 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA. 


481 


tissues  surrounding  the  acute  abscess.  At  times  the  only  evidence  of 
a  fistula  is  a  small  spot  of  inflammation  surrounding  a  minute  opening 
from  which  pus  exudes.  The  fistula  is  sometimes  located  upon  the 
lingual  surface  of  the  gum.  It  may  perforate  the  bone  of  the  hard 
palate  and  open  through  the  mucous  membrane  of  the  roof  of  the 
mouth  (Fig.  431).  Instead  of  finding  exit  by  a  direct  path  through 
the  buccal  or  lingual  alveolar  plate  and  gum  the  pus  may  burrow 
along  the  length  of  the  pericementum  and  discharge  at  the  neck  of 
the  tooth.    One-half  or  more  of  the  lateral  aspect  of  the  pericementum 


Fig.  433. 


Fig.  434. 


Fistula  passing  down  through  the  body  of  the  lower 
maxilla.     (Black.) 

may  remain  vital,  although  involved  in 
a  chronic  inflammation,  the  remainder 
being  destroyed.  Not  infrequently  the 
pus  burrows  along  the  surface  of  the 
bone  and  discharges  at  a  point  over 
an  edentulous  portion  of  the  jaw. 
This  is  common  to  a  lower  bicuspid. 
Where  the  apices  of  the  roots  of 
upper  posterior  teeth  lie  in  very  close 
proximity  to  the  floor  of  the  antrum, 
perforation  of  this  floor  may  occur 
before  tissue  destruction  has  proceeded  far  enough  in  other  directions 
to  afford  escape  to  the  pus  (Fig.  423).  Extensive  pus  accumu- 
lations may  occur  in  the  antrum  in  consequence.  It  may  dis- 
charge into  the  nasal  cavity,  in  connection  with  acute  abscess;  at  such 
points  the  discharge  may  remain  persistent.  Somethnes  the  discharge 
occurs  through  the  canal  of  the  affected  tooth;  the  condition  then 
becomes  one  of  blind  abscess  (Fig.  418).  Upon  a  lower  tooth,  par- 
ticularly the  incisors,  the  pus  may  burrow  downward  through  the 

31 


Chronic  alveolar  abscess  of  the  root  of 
the  lower  incisor,  with  abscess  cavity 
passing  through  the  body  of  the  bone 
and  discharging  on  the  skin  beneath  the 
chin  :  a,  very  large  abscess  cavity  ;  6, 
mouth  of  the  fistula.     (Black.) 


482 


DISEASES  OF  THE  PERICEMENTUM. 


cancellated  tissue  of  the  bone  and  emerge  at  the  base  of  the  bone 
and  open  upon  the  face  (Figs.  433  and  434). 

In  other  cases  the  pus  may  perforate  the  bone,  and  find  passage 
along  the  submuscular  tissue,  opening  upon  the  face  or  neck  (Fig. 
435).  The  apices  of  the  roots  of  teeth  lying  beneath  the  line  of  in- 
sertion of  the  mylohyoid  muscle  may  cause  an  abscess  to  open  in  the 


Fig.  43.5. 


Fig.  436. 


Chronic  alveolar  abscess  at  the  root  of 


Abscess  with  tortuous  sinus,  opening  upon  the 
face :  A,  tissue  of  cheek ;  B,  floor  of  mouth  ;  C,  ab- 
scess tract. 


neck  cavity.  Cryer  records  a  case 
where  an  abscess  opening  upon  the 
face  immediately  anterior  to  the  line 
of  the  facial  artery  was  traced  to  the 
root  of  a  lower  molar;  the  direction  of 
the  sinus  is  shown  in  Fig.  436.     In  a 


a  lower  incisor,  with  a  fistula  discharging    CaSC   haVUlg  a  Similar  anatomiCal  aSSO- 

on  the  face  under  the  chin:  a,  abscess  ciation,  the  pus  penetrated  the  bone 

cavity  in  the  bone;  o.  b,  b,  fistula  follow-      . 

ing  in  the  periosteum  down  to  the  lower    liugually,  WaS  Cncapsulcd   beneath  the 

margin  of  the  body  of  the  bone  and  dis-    •    x  i  .  •  j  i  j 

charging  on  the  skin.    (Black.)  mtcmal    pterygoid   musclc,    and    ap- 

peared as  a  swelling  at  the  inner  as- 
pect of  the  angle  of  the  jaw.  Occasionally  the  apices  of  the  roots  of 
lower  molars  are  separated  from  the  inferior  dental  canal  by  only 
a  thin  lamina  of  bone,  so  that  discharge  into  this  canal  may  occur 
with  infiltration  along  the  vessels  and  nerves  in  the  canal  (Fig.  240). 
While  discharge  into  the  nasal  chamber  is  most  frequently  associated 
with  abscess  upon  the  central  incisors,  abscesses  upon  molars  may 
discharge  into  the  same  cavity. 

Cementum  infection  occurs  as  a  sequence  to  death  of  the  cement 
corpuscles  from  lack  of  nutrition.  Pus  calculi  may  also  form  on  the 
roots  in  the  long-continued  cases.     The  granulation  tissue  springing 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA. 


483 


up  about  the  parts  has  a  resorbent  action  and  the  root  ends  are  often 
resorbed,  though  this  action  is  probably  to  an  extent  counteracted  by 
the  alkalinity  of  the  pus.  The  formation  of  the  latter  may,  however, 
be  in  abeyance  at  times. 

The  extent  of  tissue  destruction  varies  considerably,  but  is  usually 
greatest  in  dependent  parts,  gravity  influencing  the  burrowing  of  the 
pus. 

Symptoms  and  Diagnosis.  A  fistula  is  seen  upon  the  gum,  visible  as 
either  a  small  teat  of  flesh  (perhaps  pedunculated),  discharging  pus, 


Fig.  437. 


Apical    abscess,   rarefied  area,   showing 
light  in  the  skiagraph.     (By  Custer.) 

or  as  a  tiny  orifice  in  the  gum 
surrounded  by  inflamed  tissue, 
and  from  which  pus  may  be 
squeezed  (Fig.  422).  As  a 
rule,  a  soft,  silver  probe  may 

Large   abscess   cavity  in   relation  with  a  lateral  ,  Tlflq<=;prl    to     thp     anex    of     a 

incisor,  complicated  by  an  impacted  supernumerary  DC     paSSCQ   tO     Xne     apex    Ul     d 

tooth  beneath  the  nasal  spine.    (Philadelphia  Dental  nearby  TOOt,    whether    pOSSCSS- 

College  Museum.)  ,  i       i  i     i    • 

1112  a  crown  or  embeaaea  m 
the  bone.  In  case  of  an  external  opening  upon  the  face  a  similar 
procedure  shows  the  trouble  to  He  with  some  tooth  root.  The  ir-ray 
will  sometimes  be  valuable  in  determining  the  exact  location  of  the 
abscess  cavity. 

Upon  the  teeth  themselves  but  four  conditions  may  cause  a  fistulous 
opening:  (1)  moist  gangrene  of  the  pulp  or  its  equivalent  apical 
infection;  (2)  septic  perforations,  apical  or  lateral;  (3)  a  pericemental 
abscess  (see  Pericemental  Abscess) ;  (4)  a  secondary  abscess  associated 
with  a  pyorrhoea  pocket.     (See  Pyorrhoea  Alveolaris.) 

Aside  from  these,  the  probe  may  lead  to  carious  or  necrosed  bone, 
a  cyst,  an  impacted  tooth,  or  a  subperiosteal  abscess  (maxillary  peri- 
ostitis). - 


484  DISEASES  OF  THE  PERICEMENTUM. 

In  these  cases  the  probe  does  not  lead  to  the  root.  Carious  bone 
will  have  a  rotten  feel  to  an  excavator,  necrosed  bone  will  be  exposed 
and  firm,  or  the  sequestrum  will  be  in  evidence  as  a  movable  body. 
There  may  also  be  several  fistulse  and  extensive  inflammation  of  the 
tissue.  A  cyst  will  be  a  tumor  with  certain  characteristics  and  an 
impacted  tooth  will  usually  impart  the  feel  of  smooth  enamel  to  the 
instrument,  though  the  enamel  may  at  times  be  rough  at  certain  points. 
An  embedded  root  will  be  movable,  and  will  present  the  dentine  and 
its  central  opening,  the  pulp  canal,  as  diagnostic  features.  Maxillary 
periostitis  will,  as  a  rule,  have  a  history  of  traumatism,  or  the  previous 
use  of  a  probably  infected  hypodermic  needle^  associated  with  it.  In 
all  cases  not  clearly  due  to  other  than  dental  causes,  evidence  of  the 
four  dental  conditions  mentioned  should  be  sought. 

Treatment.  In  cases  arising  from  sources  not  dental,  surgical  inter- 
ference for  the  removal  of  the  cause  is  necessary.  This  may  require 
a  minor  or  major  operation,  according  to  the  case.  In  some  cases 
radical  operation  may  not  be  advisable. 

In  the  purely  dental  cases  the  cause  must  also  be  removed.  If 
due  to  pericemental  abscess  this  is  to  be  treated.  If  due  to  a  septic 
perforation  not  yielding  to  treatment  by  way  of  the  root  canal 
the  fistula  may  be  enlarged,  packed  open  with  antiseptic  cotton  or 
gauze  applied  on  successive  days,  and  when  the  perforation  is 
exposed  it  may  be  filled  with  amalgam.  If  properly  done  the 
fistula  should  heal.  If  this  operation  be  impossible  the  root  should 
be  amputated  at  a  point  between  the  perforation  and  the  crown.  If 
the  perforation  be  in  the  middle  or  cervical  third  of  the  root  it  may 
at  times  be  treated  from  the  root  canal.  If  incurable  the  entire  root 
must  be  amputated  in  case  of  a  multirooted  tooth.  In  case  of  a 
single-rooted  tooth  the  tooth  must  be  extracted,  and  if  the  conditions 
warrant  the  operation  the  root  may  be  perfectly  sterilized,  properly 
filled,  and  then  replanted  after  the  associated  abscess  cavity  has  been 
surgically  obliterated. 

In  the  cases  due  to  moist  gangrene  of  the  pulp  the  canals  must  be 
freely  entered,  the  apical  foramen  opened  with  Donaldson  or  other 
cleansers,  and  the  canals  and  abscess  tract  thoroughly  sterilized. 

The  canals  are  sterilized  with  sodium  dioxide  freely  used.  The 
canal  is  flooded  with  3  per  cent,  hydrogen  dioxide  and  with  a  Swiss 
broach  upon  which  cotton  is  wound ;  a  plunging  force  is  exerted  upon 
the  fluid  in  the  canal.    This  tends  to  drive  it  into  the  abscess  cavity 

1  Boenning,  Dental  Cosmos,  1902. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA. 


485 


and  out  of  the  fistula,  flushing  and  steriHzing  the  abscess  tract.  This 
is  then  repeated.  If  this  simple  procedure  be  not  effective,  a  thread 
of  cotton  saturated  with  hydrogen  dioxide  should  be  placed  in  the 
canal.     Pressure    is   then  exerted  with    vulcanizable  rubber,   as    in 


Fig.  439. 


Fig.  440. 


Minim  syringe. 


J.  N.  Fai-rar's  alveolar-abscess  syringe. 


pressure  anesthesia.  A  third  method  consists  of  filling  the  crown 
cavity  with  gutta-percha  or  vulcanite  rubber,  forcing  the  nozzle  of 
an  abscess  syringe  through  the  mass,  and  driving  down  the  piston  of 
the  syringe.  In  all  these  procedures  except  the  initial  steriHzation 
the  unaffected  roots  of  multirooted  teeth  are  to  be  avoided  as  far  as 


486  DISEASES  OF  THE  PERICEMENTUM. 

possible,  as  undue  pressure  may  excite  an  abscess.  The  fistula  will 
admit  the  nozzle  of  the  syringe,  which  may  be  used  to  flush  out  the 
abscess  tract  with  hydrogen  dioxide. 

All  preliminary  work  having  been  done  as  well  as  possible,  phenol- 
camphor,  carbolic  acid,  or  an  essential  oil  is  to  be  pumped  into  the 
abscess  tract  and  the  canal  temporarily  stopped  with  the  same  anti- 
septic on  cotton.  With  this  treatment  the  discharge  of  pus  should 
cease  and  be  replaced  by  serum ;  in  a  week  or  two  the  fistula  should 
have  healed  if  attached  to  treatable  canals;  for  the  difficult  canals 
subjected  to  antiseptics  only,  more  time  may  be  required. 


Bulb  syringe. 

In  the  case  of  a  recently  formed  fistula  or  large  abscess  cavity,  a  bit 
of  floss  silk  dipped  in  carbolic  acid  or  a  tent  of  antiseptic  gauze  should 
be  packed  into  the  fistula  to  keep  it  open,  in  order  that  the  abscess 
may  heal  from  the  bottom.  This  is  a  surgical  principle  established 
for  all  ulcers  with  small  openings  which  tend  to  heal  over  confined 
pus.  If  the  abscess  cavity  does  not  heal,  one  of  several  causes  may 
be  assigned:  (1)  the  crypts  in  the  walls  of  the  abscess  cavity  may 
require  further  disinfection;  (2)  the  cotton  in  the  canal  may  have 
absorbed  pus  formed  after  an  interval  of  antiseptic  influence  and  may 
keep  up  the  infection;  (3)  the  root  end  may  be  incrusted  with  calculus, 
or  the  cementum  be  infected,  or  dead  bone  may  be  present;  (4)  the 
root  canal  may  not  be  explorable. 

For  the  first  condition  the  canal  and  abscess  tract  may  be  treated 
with  10  per  cent,  zinc  chloride,  or  mercuric  chloride  may  be  added  to 
hydrogen  dioxide  (1 :  500  or  1 :  1000)  and  the  abscess  cavity  syringed 
out  at  intervals.  For  the  second  condition  a  non-absorbent  dressing 
should  be  used,  such  as  Forma-Percha,  or  the  root  apex  may  be  perma- 
nently filled  with  gutta-percha.  In  the  fine,  unexplorable  canals, 
25  per  cent.  p}T:ozone  may  be  used  for  twenty-four  hours  as  though 
bleaching  the  root,  or  Rhein's  or  Bethel's  cataphoric  methods  may  be 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA.  437 

employed.  In  some  cases  abscesses  require  some  weeks  to  heal,  but 
eventually  do  so,  particularly  if  the  abscess  be  syringed  out  with  an 
antiseptic  every  third  day  via  the  fistula. 

Tissues  about  abscesses  have  an  inherent  tendency  to  regeneration; 
cases  of  long  standing  frequently  healing  promptly,  sometimes  though 
not  often  in  twenty-four  hours. ^ 

For  the  third  class  of  cases  the  root  and  fistula  should  be  syringed 
with  aromatic  or  25  per  cent,  sulphuric  acid.  The  root  apex  should 
be  sealed  with  gutta-percha  and  the  abscess  tract  syringed  once  a  week 
with  the  25  per  cent,  sulphuric  acid,  the  mouth  and  clothing  being 
properly  protected  by  using  a  pad  of  cottonoid  over  the  fistula  and 
needle  to  absorb  the  excess.  This  dissolves  calculi  and  disinfects  dead 
cementum.  It  also  stimulates  the  soft  parts  to  a  granulative  action. 
If  necessary  the  patient  should  receive  appropriate  systemic  treatment. 
In  this  way  some  old  and  somewhat  obstinate  cases  may  be  induced 
to  heal.  If  the  abscess  be  incurable  by  the 
above  method,  or  radical  measures  being 
considered  better,  the  root  end  may  be 
amputated.  The  fistula  is  enlarged  and 
packed  open  with  antiseptic  gauze  applied 
until  the  root  end  is  fairly  in  view.  After 
sterilization  of  the  abscess  cavity  and  local 
anaesthesia,  a  dentate  fissure  bur  is  laid  upon 
one  side  of  the  root  at  the  level  of  the  healthy 

,  •     1     1  11  •  1  •  Amputation  of  root  apex:  06, 

tissue,  and  carried  laterally  with  a  sawing  opening-  in  the  gum  made  by 
motion  until  the  root  end  is  separated.     It  packing  fistula ;  ac,  abscess  cav- 

^  ity  ;  EF,  root  filling. 

may  readily  be  picked  out.    If  the  root  can 

be  correctly  located  before  packing  the  fistula  the  part  may  be  anaes- 
thetized and  a  portion  of  gum  may  be  cut  away  with  a  tubular  knife 
or  an  incision  may  be  made,  after  which  a  fissure  or  surgical  bur  may 
be  used  to  cut  away  the  root.  Any  necrosed  bone  may  be  removed 
in  the  same  manner  by  the  use  of  sterilized  burs. 

Necrosed  root  ends  may  occasionally  be  seen  projecting  through  the 
gum  and  alveolar  process  which  have  been  lost  above  them.  They 
should  be  removed  as  above  indicated. 

Antiseptic  gauze  should  be  packed  into  the  abscess  cavity  to  stim- 
ulate granulation  activity.  The  quantity  of  gauze  should  be  gradually 
lessened  until  the  cavity  is  nearly  healed.  It  should  thereafter  be  kept 
sterihzed  by  means  of  hydrogen  dioxide  until  the  cavity  has  healed. 

1  Darby,  Proceedings  Academy  of  Stomatology,  Philadelphia,  1899. 


488 


DISEASES  OF  THE  PERICEMENTUM. 


Stimulation  by  means  of  fused  silver  nitrate  is  at  times  necessary. 
Bone  should  gradually  be  deposited  about  the  roots  (Figs.  443,  444  and 
445).  Failure  indicates  some  condition  of  sepsis;  presumably  the  ampu- 
tation has  not  included  all  septic  root  or  the  canal  filling  is  defective. 
A  still  more  radical  method  of  surgical  treatment  involves  the 
extraction  and  replantation  of  the  root.  The  mouth  is  sterilized  and 
the  tooth  extracted,  care  being  taken  not  to  injure  the  enamel  with 
the  forceps.  It  is  then  placed  in  a  1 :  1000  solution  of  mercuric  chloride 
at  120°  F.  The  apex  of  the  alveolus  is  in  the  mean  time  sterilized 
with  hydrogen  dioxide  plus  mercuric  chloride  and  thoroughly  curetted. 
Bleeding  is  checked  with  the  same  solution  or  adrenalin  chloride,  and 
a  tampon  of  cotton  saturated  with  a  20  per  cent,  solution  of  phenol- 
sodique  is  packed  into  the  alveolus. 


Fig.  445. 


Fig.  443. — A  skiagraph  of  apical  abscess  cavity  about  two  root  apices;  incurable  by 
ordinary  means. 

Fig.  444. — The  same  after  root  amputation. 

Fig.  445.— The  same  thirty  days  later,  showing  a  certain  amount  of  new  bone  formation. 
(Price.) 

Returning  to  the  tooth  the  apex  is  cut  off  slightly  beyond  the  denuded 
area  and  smoothed;  the  pulp  canal  is  well  opened  from  the  apex,  all 
debris  removed  from  it,  and  it  is  then  well  sterilized  with  sodium 
dioxide  or  25  per  cent,  pyrozone,  or  both.  The  canal  is  then  dried 
and  filled  entirely  with  gutta-percha,  or  partly  with  gutta-percha,  and 
the  operation  completed  with  gold,  which  is  nicely  smoothed.  The 
root  should  be  handled  in  an  aseptic  napkin  or  one  wet  with  the 
antiseptic,  and  when  ready  should  be  returned  to  the  sterilizing  solution. 
All  being  ready  the  tampon  is  removed,  the  tooth  replaced  in  its  socket, 
and  a  previously  prepared  retaining  appliance  cemented  to  place. 
This  should  remain  from  three  to  six  weeks  and  be  replaced  should 
indications  demand  it.  If  the  tooth  be  valueless  for  replantation 
purposes,  the  operation  of  transplantation  may  be  done  either  imme- 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA.  489 

diately  after  extraction  of  the  offending  tooth  or  a  few  days  later. 
The  possibiHty  of  resorption  of  the  root  after  plantations  should  have 
careful  consideration,  though  it  is  not  prohibitory. 

Several  cases  of  fistulous  openings  into  the  antrum  have  been  noted 
by  canal  exploration  in  which  no  history  of  discomfort  from  antral 
empyema  could  be  obtained.  It  was  assumed  that  the  root  ends 
approximated  the  floor  of  the  antrum,  and  that  the  abscesses  were 
of  simple  chronic  type.  Such  cases  were  treated  upon  the  common 
principle  of  canal  antisepsis,  flushing  the  abscess  tract  with  hydrogen 
dioxide,  and  filling  the  canals.  The  antral  condition  was  explained 
to  the  patients,  who  were  warned  of  possibilities,  but  such  as  yet  have 
not  been  reported. 

A  chronic  abscess  may  discharge  into  the  maxillary  sinus  for  a 
long  period  before  being  discovered,  unless  the  pus-accumulation  be 
extensive,  when  it  escapes  from   the 

,  -PI  Fig.  446. 

antrum  into  the  cavity  of  the  nose, 
discharging  by  one  side.  Smaller  ac- 
cumulations of  pus  find  exit  in  the 
recumbent  position,  and  attention  is 
called  to  one  antrum  as  the  seat  of 
affection  by  noting  that  in  the  morning 
pus  appears  at  but  one  nostril.  The 
discharges  from  purulent  nasal  catarrh 
appear  upon  both  sides. 

A    more     common    history    of     antral        Empyema   of    antrum   due   to  abscess 

empyema   is   the   patient's    complaint   upon  root  of  bicuspid  tooth.    (Radio- 

rJ  tr  r  graph  by  Price.) 

of  dull,   heavy  pains   and   uneasiness 

over  one  side  of  the  face,  and  an  offensive  odor,  which  may  not  be 
evident  to  the  operator.  High  transillumination  of  the  tissues  about 
the  mouth  and  through  the  cheek  by  means  of  the  electric  mouth- 
mirror  may  reveal  an  opacity  on  one  or  perhaps  both  sides,  indicat- 
ing the  presence  of  fluid  in  the  antrum.  Examination  of  the  pos- 
terior teeth  will  show  one  of  them  to  be  pulpless.  If  such  a  tooth  be 
extracted,  a  profuse  flow  of  pus  may  follow,  and  a  probe  may  be 
passed  through  an  alveolus  directly  into  the  antrum.  It  is  to  be 
remembered  that  antral  empyema  may  occur  from  the  influenza 
bacillus  in  the  blood.  It  has  been  noted  in  connection  with  la  grippe. 
The  aj-rays  are  valuable  diagnostic  means  (Fig.  446) . 

Although  extraction  is  the  usual  surgical  relief,  dental  conservatism 
rebels  against  the  immediate  condemnation  of    the  offending  tooth. 


490  DISEASES  OF  THE  PERICEMENTUM. 

Efforts  at  curing  the  antral  condition  through  the  pulp  canal  are 
well-nigh  hopeless — the  antrum  is  entered  at  some  other  point.  The 
tooth  is  treated  as  any  infecting  root;  is  sterilized  and  filled.  The 
most  certain  spot  of  entry  to  the  antrum  is  about  one-quarter  inch 
above  the  buccal  roots  of  the  upper  first  molar.  The  part,  or  the 
patient,  is  anaesthetized,  and  the  soft  tissues  incised  or  a  section 
removed  by  means  of  a  tubular  knife;  a  drill  or  trephine  at  least  one- 
eighth  inch  in  diameter,  driven  rapidly,  is  passed  upward,  backward, 
and  inward,  piercing  the  thin  shell  of  the  antrum  at  this  point.  The 
nozzle  of  an  atomizer,  filled  with  a  3  per  cent,  solution  of  pyrozone, 
which  has  been  rendered  alkaline  by  sodium  dioxide  and  w^armed,  is 
passed  into  the  antrum  and  the  cavity  is  freely  sprayed.  A  probe  is 
passed  into  the  cavity  and  an  exploration  made  to  detect  the  presence 
of  any  dead  bone,  which,  if  found,  must  be  removed,  the  ca"saty  of 
entrance  being  enlarged  to  permit  its  removal.  After  operation  the 
cavity  is  packed  with  nosophen  or  other  gauze  until  granulation  is 
stimulated,  after  which  the  cavity  is  sprayed  about  every  other  day 
with  very  dilute,  warm  Dobell's  solution.  (For  further  information  see 
works  on  oral  surgery.) 

Unless  much  necrosis  of  bone  occur  cases  of  fistula,  opening  upon 
the  face  or  neck,  may  be  healed  by  the  ordinary  methods  carried  out 
with  extraordinary  care  to  accomplish  the  irrigation  of  the  fistula. 
The  scar  formation  is  less  than  when  extraction  is  practised  for  the 
removal  of  the  cause.  If  the  fistula  be  indolent  the  granulations  may 
be  stimulated  by  means  of  an  injection  of  10  per  cent,  silver  nitrate 
solution.  If  the  fistula  obstinately  refuse  to  heal  the  tooth  should  be 
extracted  and  necrosed  bone,  if  any  be  present,  surgically  removed. 

Flagg^  suggested  as  a  means  of  lessening  scar  formation  that  a  seton 
be  passed  through  the  external  fistula  into  the  mouth,  and  that  it  be 
gradually  drawn  into  the  mouth  as  the  external  fistula  heals,  after 
which  the  tooth  is  to  be  extracted. 

In  fistulse  discharging  upon  the  face  the  formation  of  scar  tissue  may 
bind  the  tissue  of  the  cheek  tight  to  the  bone.  AMien  this  occurs 
beneath  the  tip  of  the  chin,  the  scar,  after  healing,  usually  resembles 
a  dimple,  and  calls  for  no  interference.  The  scar  and  binding  down 
along  the  border  of  the  inferior  maxilla,  or  beneath  the  malar  bone 
in  the  upper  maxilla,  may  produce  deformity  calling  for  remedy  (Figs. 
447  and  448).  Black's  operation  is  to  be  performed  to  lessen  the 
deformity,  for  its  complete  correction  is  not  practicable.     A  finger 

1  Lectures  on  Dental  Therapeutics. 


BONE  IXFECTIOX  ASSOCIATED  WITH  DENTAL  LESIONS.     491 

placed  in  the  mouth  draws  the  cheek  away  from  the  alveolar  wall,  when 
the  exact  position  of  the  cord  of  attachment  is  discovered.  A  tenotome- 
knife  is  passed  into  the  tissues,  di^dding  the  band  of  attachment;  a  long 
pin  is  passed  through  the  most  depressed  portion  of  the  scar,  its  centre, 
the  long  ends  of  the  pin  resting  upon  the  face;  strips  of  adhesive  plaster 
laid  upon  the  skin  under  the  head  and  point  of  the  pin  T^-ill  prevent 
the  latter  sinking  into  the  soft  tissues.  The  pin  is  retained  for  several 
days,  until  the  cut  in  the  mouth  heals. 


BONE   INFECTION  ASSOCIATED    WITH   DENTAL  LESIONS. 

During  the  course  of  acute  and  chronic  abscess  the  bone-marrow 
becomes  inflamed  by  the  pyogenic  organisms  and  is  broken  doTvm 
into  pus.  The  condition  may  continue  after  extraction  for  apical 
abscess  in  the  second  stage.     It  may  also  occur  from  the  bruising  of 

Fig.  447.  Fig.  448. 


Scar  caused  by  alveolar  abscess  discharj 
ing  on  the  face.     (Black.) 


Operation  for  the  remedy  of  scar  on  the  face 
caused  by  alveolar  abscess.     (Black.) 


the  periosteal  lining  of  the  alveolus  as  the  result  of  extraction  of  a 
hypercementosed  root,  or  from  a  bruise  induced  by  forcible  use  of 
forceps  in  the  removal  of  deeply  seated  roots. 

The  walls  of  the  alveolus  become  infected  by  pyogenic  organisms, 
among  which  the  diplococcus  pneumoniae  figures  prominently.  (See 
p.  98.) 

The  lea\dng  of  cotton  tampons,  placed  as  vehicles  for  pam-relie^ing- 
agents,  for  an  undue  length  of  time  also  invites  infection. 

If  during  extraction  the  alveolar  margins  be  lacerated,  and  espe- 


492  DISEASES  OF  THE  PEEICEMEXTUM. 

cially  if  the  bone  be  uncovered  by  clot,  it  also  becomes  infected. 
Ratiijed  gum  margins  become  gangrenous. 

Symptoms.  The  symptoms  are  those  of  local  inflammation  without 
necessarily  much  swelling  of  contiguous  tissues,  such  as  occurs  in  acute 
abscess.  If  due  to  an  acute  abscess  in  the  second  stage,  however,  the 
symptoms  of  that  condition  may  continue. 

In  the  majority  of  cases  the  pain  is  of  a  deep,  boring,  continuous 
character.  Reflex  pains  are  also  produced.  Much  debility  is  caused 
by  the  wearing  character  of  the  pain,  the  loss  of  sleep  and  appetite, 
and  probably  also  because  of  absorption  of  toxins.  The  gum  margins 
are  perhaps  sloughing;  the  bone  may  be  exposed  and  exquisitely 
painful  to  touch,  or  it  may  be  necrotic  and  insensitive  superficially. 

If  the  suppuration  extend  deeply  into  the  bane  the  contiguous 
tissues  are  inflamed;  in  some  cases  widely  so.  Cases  of  general  septi- 
cfemic  or  pysemic  infection  from  this  sourpe  have  been  recorded. 

Treatment.  The  mouth  and,  in  so  far  as  possible,  the  inflamed  part 
must  be  sterilized.  Probably  mercuric  chloride  in  hydrogen  dioxide 
(1 :  1000)  will  answer  best. 

An  injection  of  a  1  or  2  percent,  solution  of  cocaine  into  the  healthy 
tissue  overlying  the  alveolus  will  assist  in  alleviating  the  acute  pain 
and  partly  anaesthetize  the  parts.  All  sloughing  gum  should  be  cut 
away.  Exposed  bone  should  be  anaesthetized  by  strong  cocaine  solu- 
tions if  painful  to  touch,  or  the  patient  should  be  anaesthetized  if 
necessary.  ^Vhether  acutely  inflamed  or  necrotic,  the  bone  should  be 
cut  away  with  large  sterile  burs  until  healthy  tissue  is  reached.  After 
washing  out  the  debris  and  further  sterilization  a  clot  is  to  be  in- 
duced by  curetting  if  necessary.  The  mouth  is  to  be  kept  sterilized 
and  the  patient  is  to  be  seen  daily  for  a  repetition  of  the  curetting. 
In  ordinary  cases  one  or  two  local  treatments  will  be  effective,  but 
the  tonic,  antiseptic,  systemic  medication  recommended  under  the 
heading  of  acute  apical  abscess  is  advised. 

If  the  infection  be  of  aggravated  character,  precautions  in  the  form 
of  suitable  systemic  medication  should  be  taken  against  a  possible 
septicaemia. 

If  the  patient  be  not  wilhng,  or  unable,  to  bear  this  operation  at  the 
first  \asit  because  of  the  demoralization  produced  by  the  pain,  an 
alternative  proceeding  may  be  adopted.  A  pellet  of  cotton  wet  with 
campho-phenique  should  be  rolled  in  powdered  orthoform  and  intro- 
duced into  the  socket  after  sterihzation  with  the  mercuric  chloride 
solution. 


NECROSIS  WITH  CHRONIC  ALVEOLODENTAL  ABSCESS.       493, 

The  repetition  of  this  after  five  to  eight  hours  will  afford  marked 
rehef.  Later  the  radical  operation  may  be  performed.  The  intro- 
duction of  cotton  or  gauze  dressings  into  the  alveoli  for  relief  of  pain 
immediately  following  extraction  is  to  be  done  only  with  extreme  care 
and  for  short  periods  only,  as  such  dressings  are  apt  to  be  left  in  place 
by  patients,  and,  becoming  septic,  act  as  causes  of  sepsis  of  the  alveolar 
process.  While  alveoli  will  fill  with  granulations  in  the  absence  of  a 
clot  filling  them,  such  a  clot  seems  to  be  the  best  protection  against 
sepsis. 

EXTENSIVE  NECROSIS  ASSOCIATED   WITH  CHRONIC  ALVEOLO- 
DENTAL ABSCESS. 

Every  chronic  alveolodental  abscess  carries  with  it  the  danger  of 
bone  complication.  It  has  been  shown  that  in  bone  infection  the 
organisms  are  highly  virulent.  Fortunately  in  most  cases  the  involve- 
ment is  slight  and  the  parts  care  for  themselves  when  the  cause  is 
removed.  In  more  aggravated  cases,  either  caries  or  necrosis  of  the 
bone  may  follow.  Pus  is  formed  at  the  expense  of  the  parts.  In 
caries  the  pus  escapes  by  several  fistulse,  and  examination  leads  to 
porous  dead  bone.  In  necrosis  there  is  circumvallation  of  a  portion 
or  portions  of  bone,  and  finally  one  or  more  sequestra  are  loosened 
and  later  in  part  liquefied.  The  remainder  gradually  works  out  of 
the  fistula  as  one  large  or  numerous  small  pieces.  The  patient  may 
be  much  debilitated.  Surprising  recoveries  of  extensively  necrotic 
parts  occur  if  the  patient  be  brought  into  good  physical  condition 
and  the  parts  are  antiseptically  treated,  the  thorough  loosening  of  the 
sequestra  being  awaited.  By  this  means  teeth  have  been  retained  in 
place  and  covered  with  new  tissue,  which  operation  would  have  exposed 
or  removed.  The  determination  of  the  point  at  which  operative  inter- 
ference is  desirable  must  depend  upon  the  particular  case  and  the 
amount  of  deformity  likely  to  result  from  the  operation. 

Honl  and  Bukovsky  are  credited  with  the  successful  treatment  of 
bad  chronic  suppurations  by  means  of  local  applications  of  pyocyaneo- 
protein.     (See  immune  proteids.) 

Jesensky^  treated  a  case  of  six  months'  standing,  incurable  by 
ordinary  antiseptic  and  systemic  treatment,  and  obtained  remarkable 
results. 

Syphilitic  intoxication  may  cause  a  necrosis  of  alveolar  bone.    The 

1  Dental  Cosmos,  1901. 


494  DISEASES  OF  THE  PERICEMENTUM. 

extent  to  which  the  teeth  or  oral  infection  act  as  active  exciting  causes 
depends  upon  the  condition  present. 

SEPTIC    APICAL    PERICEMENTITIS    COMPLICATED   BY  PER- 
FORATION. 

In  the  treatment  of  root  canals  the  required  mechanical  work  some- 
times results  in  (1)  the  passage  of  the  drill  through  the  apical  foramen, 
enlarging  it;  (2)  through  the  side  of  the  root,  causing  a  perforation. 

In  the  first  variety  the  complication  chiefly  concerns  the  root  filling, 
which  is  to  be  conducted  after  sterilization  upon  the  same  plan  as 
for  filling  an  unformed  foramen.     (See  p.  436.) 

If  a  lateral  perforation  be  made  near  the  root  apex,  it  may  be  filled 
after  sterilization  with  a  cone  similarly  applied,  but  made   bevelled 


Skiagraph  of  crowned  curved  root,  with  per-  Showing  the  relations  of  an  abscess  upon 

loration  and  protruding  root  filling  near  apical  a  temporary  tooth,  with  the  crown  of  a  de- 

loramen,'«-ith  septic  conditions,  would  require  veloping  pei-manent  tooth  underlying  it. 
root  amputation.     (Price.i) 

at  the  end  or  a  bit  of  aseptic  sponge  may  be  introduced  against 
the  tissue  for  a  base  and  be  covered  by  oxychloride  of  zinc.  If 
septic  conditions  persist  the  root  end  must  be  amputated,  or  the 
tooth  extracted,  prepared,  and  replanted.  If  made  in  the  middle 
third  of  the  root  the  canal  must  be  sought  for  and  treated  as  usual 
beyond  the  perforation,  which  is  then  separately  treated  with  a 
gutta-percha  cone,  or  a  plaque  of  gutta-percha  may  be  laid  over 
the  perforation  and  antiseptic  cements  or  copper  amalgam  used 
to  secure  it  in  position  (Fig.  401).  Amputation  or  extraction  and 
replantation  may  be  resorted  to.  In  a  favorable  case  after  canal 
exploration  a  tapering  probe  may  be  passed  into  the  canal  and 
copper  amalgam  gently  tamped  about  it  and  against  the  perforation, 
the  probe  is  then  withdrawn,  leaving  a  central  canal  which  is  later 

1  Items  of  Interest,  1901. 


CHRONIC  SEPTIC  APICAL  PERICEMEXTITIS.  495 

treated.  Girdwood  has  reported  good  results  from  the  use  of  copper 
amalgam  which,  in  this  connection,  the  writer  can  confirm. 

Chronic  Septic  Pericementitis  in  the  Temporary  Teeth.  Any  of 
the  chronic  septic  conditions  described  may  occur  upon  the  temporary 
teeth.  The  presence  of  resorption  and  of  the  permanent  crown  usually 
confines  the  inflammation  to  a  point  lower  in  the  alyeolar  process 
than  in  the  case  of  permanent  teeth.  The  loose  character  of  the 
structure  causes  the  ulceration  to  occupy  a  larger  area,  and  the  parts 
in  chronic  inflammation  look  more  angry,  but  are  fairly  well  tolerated. 
The  treatment  is  practically  the  same  for  the  curable  cases;  the 
others  should  be  extracted.  The  root  canals  when  treated  should  be 
filled  with  absorbable  materials  such  as  paraffin  or  wax  combined 
with  aristol  (Fig.  450). 

Johnson^  suggests  that  a  eucal\'ptol  solution  of  gutta-percha  (see 
p.  437)  be  pumped  into  the  canals  and  pressure  exerted  with  tempo- 
rary stopping  until  the  solution  appears  at  the  fistula.  The  temporary 
stopping  that  does  not  interfere  with  filling  integrity  should  be  left. 

Chronic  Septic  Apical  Pericementitis  (Non-purulent).  Continued 
inflammation  of  a  low  grade  (interstitial  gingiyitis),  or  what  may  in 
reality  be  continued  atonic  hypersemia,  may  exist  in  the  apical  peri- 
cementum for  long  periods  without  pus  formation. 

Cause  and  Pathology.  The  cause  consists  of  unremoyed  gangrenous 
pulp  tissue,  septic  serous  collections  in  canal  apices  or  about  imperfect 
root  fillings,  or  septic  material  in  the  root  tubuli. 

Albuminous  fluid  may  enter  the  canal  via  the  apical  foramen  and, 
becoming  infected,  putrefaction  ensues.  The  source  of  infection  may 
possibly  be  the  blood,  but  leaky  crown  and  root  fillings  more  probably 
permit  bacteria  to  enter  from  the  mouth.  The  more  or  less  constant 
result  of  filling  roots  with  cotton  permeated  with  eyanescent  materials 
only  is  eyidence  of  this.  The  cotton  absorbs  fluid  either  from  about 
leaky  fillings,  too  often  placed  in  contact  with  it,  or  else  from  the  apical 
tissues ;  infection  readily  occurs  and  a  highly  odorous  cotton  is  remoyed 
because  of  the  apical  irritation.  ^Yhen  the  cotton  is  well  placed  and 
confined  under  tight  sealing  materials  to  the  apical  half  of  the  root 
canal,  this  result  is  long  delayed  in  many  cases.  Portions  of  gangrenous 
pulps  remaining  in  canals  may  likewise  become  infected.  Extra  and 
untreated  canals  are  frequently  causes. 

Miller^  has  shown  that  root  tubules  are  infected  only  for  a  short 
distance  at  their  canal  ends,  so  that  infection  from  the  pericementum 

1  Dental  Cosmos,  1899.  -  Ibid. 


496 


DISEASES  OF  THE  PERICEMENTUM. 


via  the  cementum  and  dentinal  tubules  is  highly  improbable  (Fig. 
452).    The  putrefaction  produces  gases  and  these  exuding  slowly  pro- 


Dentine  from  the  root  of  an  abscessed  tooth ,  show- 
ing the  penetration  of  cocci  to  a  depth  of  about 
i/io  mm.  (V250  in.) ;  the  side  a-b  bordered  upon  the 
canal.    X  1000.     (Miller.) 


duce  the  irritation.  If  pyogenic  organ- 
isms be  present,  apical  abscess  may  at 
any  time  supervene. 

Symptoms.  Subacute  inflammation 
of  apical  tissue  being  present,  the 
symptoms  of  this  condition  are  ten- 
derness upon  decided  pressure  or  upon 
percussion;  the  response  may  only  be 
elicited  by  pressure  or  percussion  in 
one  direction.  The  tooth  gives  a  dull 
note  upon  percussion  and  is  usually 
looser    than  its   neighbors.     The  red 

Sector  of    a    cross-section  from   a  dis-    ,.  «     ,  1      p        i 

eased   root:    o,   cementum;    b,   stratum    ImC  of  the  gUm  CXtCuds  farther  tOWard 

ErdT4irx'^?r^'^'"'"^^^  the  gum  margin  than    normal-quite 

to  it  in  some  cases. 
Some  slight  looseness  may  be  noted  and  the  patient  is  apt  to  avoid 
the  tooth  in  mastication.     In  some  cases  acute  reflex  pains  in  other 
teeth  may  precede  an  outbreak  of  purulent  pericementitis,  a  frequent 


CHROXIC  SEPTIC  APICAL  PERICEMEXTITIS.  497 

sequel  to  this  condition.  There  are  also  evidences  of  pre\'ious  devital- 
ization of  the  pulp  in  opacity,  lack  of  response  to  tests  for  vitality,  etc. 
At  times  a  history  of  previous  canal  treatment  may  be  obtained  or  the 
evidences  of  an  attempt  at  canal  filling  may  be  seen  upon  opening  the 
tooth. 

Diagnosis.  The  condition  requires  careful  differentiation  from 
(1)  apical  pericementitis  due  to  traumatism  or  malocclusion;  (2) 
pericemental  abscess  in  the  early  stage;  (3)  abscess  of  the  pulp  in  the 
later  stages.  In  all  these  cases  the  pulp  may  be  vital.  Being  itself 
only  subsequent  to  death  of  the  pulp,  tests  for  vitality  are  made.  (See 
p.  445.)  If  pulp  death  be  indicated  by  the  tests  the  pulp  canal  is 
explored  and,  if  found,  filled;  a  septic  condition  about  or  beyond  the 
same  is  looked  for. 

Treatment.  The  condition  being  analogous  to  that  of  moist  gangrene, 
the  treatment  is  the  same.  Before  it  can  be  applied  the  root  canals 
should  be  opened,  and  to  accomplish  this  all  root  fillings  involved 
require  removal.  If  an  extra  canal  be  found  after  apparently  con- 
scientious work  has  been  done,  this  should  receive  attention  before 
removing  root  fillings. 

The  bulk  of  gutta-percha  root  fillings  are  best  drilled  out  with 
Gates-Glidden  drills  revolved  in  the  engine  hand-piece.  '\\Tiere  they 
extend  beyond  the  reach  of  the  finest  drill  the  Downie  broach  may  be 
used,  or  the  Swiss  broach  may  be  used  to  drive  eucalyptol  into  the 
gutta-percha  to  dissolve  it. 

All  cement  fillings  are  removed  by  a  drill  so  far  as  can  be  safely 
done,  dryness  being  a  great  aid  in  locating  the  cement  in  the  canal. 
When  the  danger  of  perforation  arises  a  stiff  Swiss  broach  may  be 
rubbed  down  to  a  drill  edge  and  used  as  a  tamp  drill.  Sulphuric  acid 
in  50  per  cent,  solution  or  aqua  ammonia  aid  by  dissolving  the  cement. 

The  object  sought  for  is  an  unfilled  canal  lumen  which,  when  found, 
is  readily  recognized  by  the  penetration  with  the  broach. 

There  can  be  no  assurance  of  safety  until  the  apical  tissue  can  be 
explored.  The  Dayton  broach  and  fine  Downie  broach  are  useful 
in  difficult  cases,  and  if  necessary  a  No.  1  Beutelrock  drill  may  be 
used.  When  the  apical  foramen  is  open  or  further  work  is  im- 
possible without  the  danger  of  perforation,  the  canal  treatment  is 
conducted  upon  the  lines  laid  down  for  gangrenous  pulp.     (See  p.  453.) 

If  the  pericementitis  have  been  of  long  standing,  the  thickening  of 
the  membrane  will  have  caused  protrusion  of  the  tooth.  The  tooth 
should  be  ground  off  at  its  point  of  occlusion  until  it  occludes  with 

32 


498  DISEASES  OF  THE  PERICEMENTUM. 

somewhat  less  force  than  its  neighbors,  the  therapeutic  principle  in 
these  cases  being  that  of  removing  the  source  of  irritation  and  procuring 
surgical  rest.  Indications  of  favorable  results  are  found  in  the  red 
gum  line  assuming  its  normal  position,  tenderness  disappearing,  and 
increased  tightness  of  the  tooth. 

This  affection  is  extremely  common  about  the  roots  of  pulpless 
teeth,  and  always  signifies  more  or  less  enforced  disuse  of  the  teeth, 
and,  if  uncorrected,  their  ultimate  loss. 

This  condition  is  sometimes  associated  with  a  chronic  swelling, 
probably  cystic  in  character,  upon  the  gum  simulating  an  acute  abscess 
in  local  appearance,  but  the  contiguous  tissues  are  not  involved.  The 
swelling  may  have  the  size  of  a  hazelnut.  Upon  treatment,  acute 
apical  abscess  is  apt  to  be  lighted  up;  therefore,  the  sterilization  by 
cataphoresis  or  by  25  per  cent,  pyrozone  should  be  prolonged  and  the 
swelling  should  be  promptly  opened  by  a  deep  incision,  thus  establish- 
ing an  artificial  fistula.  In  one  case  of  one  year's  standing,  associated 
with  a  lower  molar  tooth  which  had  a  leaky  gutta-percha  crown  and 
partial  canal  filling,  extraction  was  advised  for  reasons  other  than 
canal  treatment.  The  cyst  then  promptly  developed  as  an  acute 
abscess,  which  shifted  its  position  toward  the  cheek  and  there  dis- 
charged without  production  of  scar. 


CHAPTER    XXII. 
NON-SEPTIC   PEEICEMENTITIS. 

Various  grades  of  pericemental  irritation,  ranging  from  a  mild 
arterial  hypersemia  to  actual  inflammation,  may  be  produced  by  non- 
septic  causes. 

The  most  satisfactory  evidence  that  inflammation  may  be  so  caused 
is  furnished  by  Talbot's  experiments  with  the  mercuriahzation  of  dogs. 
Beginning  with  healthy  pericementi  these  were,  after  mercuriahzation 
of  the  animal,  found  to  contain  the  round-celled  infiltration  character- 
istic of  inflammation,  and  no  bacteria  could  be  found.  Further  e"\adence 
is  given  by  the  usual  experimental  study  of  inflammation  with  the 
mesentery  of  the  frog.  Simple  irritation,  even  with  antiseptic  sub- 
stances, produces  the  phenomena.  Any  of  the  causes  which  may 
produce  inflammation  may,  if  acting  in  more  mild  degree,  produce 
arterial  hypersemia.  If  the  action  of  the.  cause  be  violent  and  then 
discontinued,  as  in  the  case  of  a  blow,  the  inflammation  resulting  is 
acute,  but  may  pass  into  a  chronic  form;  but  if  the  cause  continue  to 
act  it  produces  a  chronic  inflammation. 

For  purposes  of  description,  non-septic  pericementitis  may  be 
divided  according  to  its  character  into  traumatic  and  symptomatic,  and 
according  to  its  location  into  apical  and  general. 

TRAUMATIC  PERICEMENTITIS. 

By  traumatic  pericementitis  is  meant  a  profound  irritation  of  the 
pericementum,  the  result  of  mechanical  violence  applied  externally  to 
the  tooth,  or  of  instrumentation  or  chemical  irritation  of  the  perice- 
mentum through  the  root  canal. 

Causes,  Violence  externally  applied  Excessive  force  delivered 
directly  upon  the  teeth,  as  in  case  of  blows,  falls,  overmalleting  in 
building  fillings,  the  biting  of  nuts,  thread,  or  other  hard  objects,  or 
force  indirectly  delivered,  as  in  case  of  blows  received  under  the  chin, 
bringing  the  teeth  forcibly  together,  may  all  cause  an  acute  peri- 
cementitis. 

An  excessive  amount  of  filling  on  the  occlusal  surface  of  a  tooth, 
a  maloccluding  crown  or  overfull  fillings  upon  the  proximal  aspect, 


500  DISEASES  OF  THE  PERICEMENTUM. 

maintaining  a  wedged  condition  cause   overocclusion  upon  the  tooth 
and  an  irritation  of  its  pericementum. 

The  overstraining  of  the  pericementum  of  a  tooth  as  the  result  of 
overuse,  as  in  cases  where  only  a  few  teeth  remain  for  mastication,  or 
where  pyorrhoea  or  calculus  has  caused  resorption  of  the  alveolar 
process  and  looseness  of  the  teeth,  or  where  artificial  dentures  are 
clasped  to  remaining  teeth,  or  where  bridges  are  supported  upon 
insufficient  piers,  are  frequent  causes  of  non-septic  pericementitis  of  a 
degenerative  character.  The  presence  of  a  rough  flaring  or  a  too 
deeply  placed  crown  band  beneath  the  gum  margins,  portions  of 
cement  used  in  cementation  of  crowns,  or  excess  of  filling  material 
beneath  the  gum  are  all  causes  of  marginal  gingivitis  with  which 
pericementitis  may  be  associated.  With  these  marginal  cases  septic 
causes  usually  have  to  be  considered  as  complications. 

Too  violent  wedging  is  always  followed  by  more  or  less  pericementitis 
of  the  wedged  teeth  and  their  neighbors,  more  marked  when  elastic- 
rubber  wedges  are  used. 

In  correcting  irregularities  of  the  teeth,  if  they  be  moved  too  rapidly, 
are  not  firmly  directed  during  the  operation,  or  subsequently  not  firmly 
maintained  in  position,  pericementitis  of  a  high  grade  is  frequently 
excited. 

Violence  Internally  Applied.  If  a  wholly  or  partially  vital  pulp 
be  torn  from  its  apical  connections,  as  in  the  use  of  pressure  ansesthesia, 
an  apical  traumatic  pericementitis  may  be  set  up.  This  is  usually 
transient. 

Excessive  laceration  of  the  apical  tissue  by  means  of  barbed  instru- 
ments; the  inclusion  of  air  or  medicament  under  a  root  dressing  or 
filling,  the  same  exercising  pressure  upon  the  apical  tissues;  the 
mechanical  irritation  of  a  projecting  root  filling,  pivot  wire,  broach  or 
drill  are  all  sufficient  causes. 

The  undue  enlargement  of  the  apex  of  the  root  canal  or  the  passage 
of  a  reamer  through  the  lateral  aspect  of  a  root  may  excite  inflam- 
mation, and  the  perfect  filling  of  the  opening  may  be  exceedingly 
difficult,  so  that  if  the  tissues  are  not  infected  at  the  time  sepsis  may 
later  follow. 

Chemical  Irritation.  The  application  of  arsenic  to  a  perforation 
may  excite  inflammation  and  necrosis.  (See  p.  429.)  The  use  of 
arsenic  as  a  pulp  devitalizer  may  cause  a  hypersemia  of  the  apical 
tissue,  causing  slight  tooth  extrusion  which  is  aggravated  by  the 
malocclusion. 


NON-SEPTIC  PERICEMENTITIS  (TRAUMATIC).  501 

The  undue  use  of  escharotics,  such  as  carboHc  acid,  sodium  dioxide, 
zinc  chloride,  sulphuric  acid,  or  mercuric  chloride,  in  a  pulp  canal 
may  excite  an  undesirable  irritation.  The  limited  irritation  following 
their  limited  use  is  often  more  than  offset  by  the  advantages  of  the 
asepsis  produced. 

Prophylaxis.  Many  of  these  causes  are  avoidable,  and  operators 
mindful  of  possible  irritations  should  avoid  the  mechanical  irritation 
of  apical  tissues,  neutralize  powerful  acids  or  alkalies,  use  escharotics 
with  caution,  wedge  teeth  gradually,  and  after  wedging  either  pack 
gutta-percha  between  the  teeth  to  permit  them  to  rest  for  a  few  days 
or  fix  them  immovably  with  wooden  wedges  or  steel  separators  during 
malleting. 

During  orthodontia,  teeth  should  be  moved  steadily  and,  after  align- 
ment is  secured,  they  should  be  firmly  maintained  in  position  until 
deposition  of  bone  occurs. 

Patients  should  be  warned  against  the  evil  effects  of  thread  biting 
and  biting  hard  substances. 

Pathology  and  Morbid  Anatomy.  Chemical  substances  applied  in 
excess  cause  a  destruction  of  tissue  dependent  upon  the  quantity  used. 
Inflammation  tending  to  the  resorption  of  the  dead  tissue  occurs.  The 
pericementitis  presumably  persists  in  some  degree  until  the  foreign 
(dead)  material  is  removed  by  natural  processes. 

In  the  case  of  protruding  foreign  bodies,  such  as  root  fillings,  broaches, 
etc.,  there  is  a  tendency  of  the  inflammation  to  become  subacute  or 
chronic.  The  foreign  body  may  to  an  extent  become  encysted,  particu- 
larly in  the  case  of  a  gutta-percha  root  filling.  In  other  cases  the  con- 
tinued vascular  disturbance,  if  of  mild  degree,  produces  hyper- 
cementosis  (see  p.  505) ;  in  more  severe  cases  resorption  of  the  root 
occurs.     (See  p.  509.) 

Cases  due  to  perforation  of  the  root  and  wounding  of  the  peri- 
cementum, after  the  acute  symptoms  have  passed,  commonly  assume 
an  irritative  and  chronic  type,  the  soft  tissues  included  in  the  perfora- 
tion being  in  a  state  analogous  to  an  ulcer.  Many  of  these  cases 
become  infected  owing  to  the  difficulty  of  completely  steriHzing  the 
apical  portion  of  the  canal  which  lies  beyond  them. 

The  pericementitis  produced  by  pressure  of  included  air,  liquid,  or 
plastic  root  filling  upon  the  apical  tissue  is  often  severe.  Upon  removal 
of  the  root  dressing  or  filling  the  engorgement  is  relieved  by  the  gushing 
of  blood  through  the  root  canal.  The  inflammation  may,  however, 
continue  unless  sedatives  be  applied  to  the  apical  tissue  via  the  canal. 


502  DISEASES  OF  THE  PERICEMENTUM. 

In  cases  due  to  traumatism,  such  as  violent  wedging,  rapid  move- 
ment in  regulating,  overmalleting,  blows,  biting  of  thread,  ice,  nuts, 
etc.,  the  condition  is  surgically  one  of  bruise. 

The  phenomena  of  active  inflammation  make  their  appearance  to  an 
extent  governed  by  the  degree  of  violence — exudation,  swelling,  red- 
ness, and  pain ;  fibrinous  and  corpuscular  exudations  occur,  and  later  a 
reorganization  of  tissue  occurs,  in  some  cases  a  degeneration,  depend- 
ing upon  the  completeness  with  which  the  indicated  therapeusis  is 
applied  and  upon  the  vitality  of  the  patient. 

Traumatic  pericementitis  in  high  degree  in  the  young  may  be 
recovered  from;  but  in  the  middle-aged  and  aged  it  may  give  rise  to  a 
series  of  degenerative  changes  which  only  end  with  the  loss  of  the  tooth. 

In  cases  due  to  looseness  of  the  teeth,  of  course,  septic  primary 
causes  have  to  be  considered,  but  the  pericementitis  may  be  quite  as 
much  mechanically  as  septically  produced. 

In  all  cases  the  extrusion  caused  by  the  inflammation  adds  another 
exciting  cause  of  apical  pericementitis — i.  e.,  malocclusion,  which 
aggravates  the  condition. 

Symptoms  and  Diagnosis.  The  amount  of  pericemental  inflamma- 
tion present  is  evidenced  by  the  soreness  and  extrusion  of  the  tooth 
and  the  degree  of  redness  in  the  overlying  gum  tissue. 

A  history  of  violence  may  be  obtained  when  it  has  occurred.  Mai- 
occlusion  may  be  detected  by  occlusion  marks  upon  fillings  or  by 
means  of  carbon  paper.  The  untoward  results  of  canal  operations 
may  be  inferred  from  a  personal  knowledge  of  the  case  or,  perhaps, 
from  the  history.  It  is  at  times  difficult  to  exclude  septic,  non-purulent, 
apical  pericementitis  as  a  cause,  particularly  if  the  case  come  from  the 
hands  of  another  practitioner.  In  doubtful  cases  the  treatment  for 
inferred  traumatisms  may  be  employed,  and  if  followed  by  good 
results  a  post  hoc  diagnosis  of  traumatic  pericementitis  may  be  made. 
The  a;-rays  afford  a  means  of  determining  extruding  root  fillings, 
broaches,  etc. 

Treatment.  Foreign  bodies  protruding  from  the  root  apex  must  be 
removed  if  persistent  symptoms  demand  it.  This  may  require  an 
artificial  opening  for  its  performance,  or  root  amputation.  Perfora- 
tions should  be  carefully  treated. 

If  e^^dence  of  pericementitis  persist,  the  end  of  the  root  including 
the  perforation  should  be  amputated  or  the  tooth  may  be  extracted,  the 
perforation  and  canal  filled  with  gold  or  gutta-percha,  and  the  tooth 
replanted  under  antiseptic  precautions. 


NON-SEPTIC  PERICEMENTITIS  {SYMPTOMATIC).  503 

In  all  cases  due  to  violence  the  treatment  is  that  adapted  to  injury; 
first,  surgical  rest  of  the  pericementum.  This  may  be  accomplished 
in  two  ways:  either  by  preventing  the  tooth  striking  its  antagonists 
or  holding  it  so  rigidly  that  it  cannot  move  if  it  does  meet  them.  As 
a  preliminary  measure  the  tooth  is  gently  but  firmly  lashed  to  its 
neighbors  by  means  of  ligatures  so  that  it  is  rigidly  held.  A  swaged 
cap  is  either  fitted  to  a  neighboring  tooth,  or  the  antagonizing  teeth  are 
ground  away  until  they  fail  to  strike  the  injured  tooth;  the  first  method 
is  to  be  preferred. 

In  cases  involving  several  teeth,  such  as  all  of  the  incisors,  two 
metallic  plates  are  quickly  swaged  to  cover  the  posterior  teeth,  and 
they  are  cemented  in  position. 

When  the  apical  tissues  have  been  irritated  by  way  of  the  canal, 
sedatives,  such  as  strong  tincture  of  aconite  or  menthol  in  chloroform  or 
menthol-phenoP  (menthol  3  parts,  carbolic  acid  1  part,  melted  together), 
should  be  applied  on  cotton  to  the  apical  tissue  by  way  of  the  root 
canal.  The  addition  of  |  grain  of  cocaine  hydrochlorate  to  one  of 
the  above  sedatives  will  notably  increase  its  action.  It  may  either 
be  rubbed  into  the  fluid  or  preferably  be  taken  up  upon  the  point  of 
the  cotton  twist  introduced  into  the  canal.  All  cases  of  traumatic 
pericementitis  require  the  persistent  use  of  counterirritants  apphed 
every  other  day  to  the  overlying  gum. 

Systemic  derivation  is  also  useful  in  the  acute  cases.  In  even  mild 
cases  not  due  to  violence  the  guarding  of  the  extruded  tooth  against 
malocclusion  is  of  advantage. 

If  the  cause  be  some  mechanical  irritant  at  the  gum  margin  this 
should  be  removed  and  the  case  treated  as  above  described.  Recogniz- 
ing the  possible  influence  of  septic  causes,  oral  antiseptics  are  to  be 
used. 

SYMPTOMATIC  NON-SEPTIC  PERICEMENTITIS. 

By  symptomatic  non-septic  pericementitis  is  meant  an  aseptic  peri- 
cementitis occurring  as  the  result  of  systemic  conditions,  or  of  the 
action  of  drugs  taken  internally. 

If  mercury  be  administered  to  patients  in  large  doses  for  long 
periods,  or  in  one  or  more  massive  doses,  or  if  the  patient  have  an 
idiosyncrasy  to  the  action  of  this  agent,  an  irritation  of  the  salivary 
glands  is  excited,  followed  by  looseness  and  soreness  of  the  teeth  and 
swelling  of  the  gums;  that  is,  a  general  pericementitis  and  maxillary 

1  Dr.  Morgan  Howe. 


504  DISEASES  OF  THE  PERICEMEXTUM. 

periostitis  arise.  Potassium  iodide  administered  in  this  condition 
relieves  the  maxillary  periostitis  and  pericementitis;  but  the  same  drug 
administered  in  health,  or  for  conditions  other  than  mercurial  poison- 
ing, also  causes  irritation  of  the  pericementum.  Pilocarpine  has  a 
similar  effect,  though  in  much  less  degree.  All  of  these  drugs  are 
partially  eliminated  by  the  glandular  appendages  of  the  mouth,  and 
during  elimination  apparently  act  as  local  irritants.  Lead  poisoning 
may  have  a  similar  action. 

Patients  who  have  a  gouty  heredity,  or  who  are  the  subjects  of 
active  gout,  frequently  exhibit  a  tenderness  of  the  entire  pericementum 
of  one  or  more  or  sometimes  all  of  the  teeth.  This  pericemental  dis- 
turbance may  be  the  precursor  of  an  acute  outbreak  of  gout  in  the 
metatarsophalangeal  joint. 

Scurvy — a  very  rare  systemic  disease — is  attended  by  rapid  de- 
generation of  the  pericementum  of  the  teeth  and  of  the  alveolar 
tissues. 

Syphilis  is  also  attended  by  pericemental  irritation.  This,  of  course, 
is  of  septic  origin. 

Talbot's  experiments  on  dogs  show  conclusively  that  a  true  peri- 
cementitis may  be  induced  owing  to  the  chemotactic  properties  of  the 
mercury  alone.     (See  Interstitial  Gingivitis.) 

In  autointoxication  by  intestinal  toxins  or  by  leucomains  in  diseases 
involving  general  malnutrition,  the  irritants  are  probably  in  part 
eliminated  by  the  gums,  which  are  in  turn  irritated.  (See  Gouty  Peri- 
cementitis.) 

It  has  been  shown  by  Loup  that  mercurial  stomatitis  may  be  cured  by 
mercury  used  as  an  oral  antiseptic;  therefore,  the  logical  conclusion  is 
that  oral  organisms  play  a  part  in  the  production  of  the  local  effects  of 
mercury;  probably  the  mercury  produces  a  local  predisposition. 

Treatment.  The  drug  should  be  discontinued,  the  disease,  if  present, 
should  be  antagonized,  and  the  local  complications,  if  any,  should  be 
appropriately  treated,  antisepsis  being  always  advisable. 

Results  of  Chronic  Non-septic  Pericementitis.  If  at  any  point  of  the 
irritated  pericementum  a  constructive  grade  of  irritation  be  maintained 
the  cemental  tissue  becomes  hypertrophied  (Fig.  454).  If  a  more 
severe  grade  of  irritation— z.  e.,  low-grade  inflammation  (interstitial 
gingivitis)— be  present  for  a  long  time,  the  cementum  and  even  the 
dentine  of  the  root  may  be  resorbed.  Both  of  these  results  may  go  on 
concurrently  at  different  points,  or  resorption  may  be  followed  by 
deposition  of  cementum  if  the  conditions  change  (Fig.  455). 


HYPERCEMEXTOSIS.  505 

Chronic  overuse  or  disuse  of  teeth  residt  in  degenerations  of  the 
pericementum  through  a  process  of  interstitial  gingivitis. 


HYPERCEMENTOSIS    (DENTAL    EXOSTOSIS,    EXCEMENTOSIS, 
HYPERPLASIA  OF  THE  CEMENTUM). 

Definition.  By  hypercementosis  is  meant  a  secondary  deposit,  or 
an  increase  of  vohime  of  the  cementum  of  a  tooth  beyond  the  normal 
limit.     It  may  be  circumscribed  or  diffuse. 

Causes.  A  mild  or  constructive  degree  of  irritation  is  the  proximate 
cause  which  may  be  excited  by  numerous  primary  causes,  such  as  a 
projecting  root  filling,  a  projecting  edge  of  crown  filling,  deposits  of 
salivary  calculus,  the  overlapping  of  a  cavity  margin  by  the  gum,  mal- 
occlusion, non-occlusion,  the  biting  of  hard  objects  such  as  nuts  or 
thread,  the  overuse  of  certain  teeth,  the  habitual  tapping  together  of 

Fig.  453. 


teeth,  the  habitual  chewing  of  toothpicks,  the  gradual  pressure  of 
gas  from  dead  pulps.  The  pressure  of  a  tooth  root  against  another 
root  during  eruption  is  a  sufficient  cause.  (See  Figs.  205  and  212.) 
The  overcrowding  of  teeth  in  an  arch  has  also  caused  this  condition. 
Chronic  alveolar  abscess  may  cause  it  by  inducing  about  itself  at  a 
distance  an  area  of  hypersemia.  Interstitial  gingivitis  is  also  a  cause. 
It  also  seems  at  times  to  be  induced  after  pulp  devitalization  from  any 
cause.  Hypercementosis  is  a  possibility  in  any  case  of  chronic  peri- 
cemental irritation;  it  represents  a  degree  of  irritation  rather  than  any 
one  specific  cause.  It  has  been  discussed  by  some  writers  under  the 
heading  of  Constructive  or  Condensing  Pericementitis. 

Situation.  Hypercementosis  may  be  diffused  over  almost  an  entire 
root  or  several  roots,  or  be  localized  as  a  distinct  nodule  at  some 
lateral  aspect,  or  exist  as  a  circumscribed  enlargement  about  the  apex 
of  a  root,  or  at  the  neck  of  a  root.  It  is  always  located  where  the 
cause  (hypersemia)  has  been  produced  (Fig.  453). 


506  DISEASES  OF  THE  PERICEMENTUM. 

Flagg  noted  that  75  per  cent,  of  cases  of  hypercementosis  were  found 
upon  posterior  teeth,  and  that  the  teeth  were  usually  of  the  character 
termed  dense — i.  e.,  the  tissues  of  the  individual  were  of  recuperative 
t}^e  tending  to  produce  constructive  changes. 

Pathology  and  Morbid  Anatomy.  For  some  time  after  eruption  the 
cementum  consists  of  but  few  lamellae  of  deposit.  It,  however,  reaches 
a  maximum  normal  development  at  which  it  normally  rests,  as  in  the 
case  of  the  physiological  pulp  cavity.  As  age  progresses  it  is  apt  to 
be  more  thickly  deposited  at  the  expense  of  the  pericementum,  which 
becomes  more  attenuated.  Whether  this  is  due  to  irritants  floating 
in  the  blood  stream,  or  to  the  various  local  irritants  above  mentioned, 

Fig.  454. 


fj^'' 


4 


nyijertrophy  of  the  cementum  on  the  side  of  a  root  of  a  lower  molar  near  the  neck  of  the 
tooth  of  a  man :  a,  dentine :  6,  cementum ;  c,  fibres  of  peridental  membrane ;  from  h  io  C  the 
cementum  is  normal  and  the  incremental  lines  fairly  regular,  but  at  d  one  of  the  lamellte  is 
greatly  thickened ;  at  e  this  lamellse  is  seen  to  be  about  equal  in  thickness  with  the  others. 
The  next  two  lamellae  are  thin  over  the  greatest  prominence,  but  one  is  much  thickened  at  jr, 
and  both  at  h.  These  latter  seem  to  partially  fill  the  valleys  which  were  occasioned  by  the  first 
irregular  growth.     From  a  lengthwise  section.     (Black.) 

or  to  perfectly  normal  development  is  not  clear  except  for  certain 
definite  cases. 

Nodular  and  irregular  forms  arising  from  the  general  surface  are 
clearly  of  abnormal  type. 

Successive  lamellae  are  deposited;  the  pericementum  recedes,  caus- 
ing resorption  of  the  alveolar  process.  Union  of  the  bone  and 
cementum  (ankylosis)  very  rarely  occurs.  A  resorption  of  cementum 
and  dentine  may  occur  at  some  point  owing  to  a  different  degree  of 
irritation,  and  in  the  area  a  new  deposition  of  cementum  may  occur 
(Fig.  455,  d).  In  some  cases  distinct  areas  of  hypercementosis  and 
root  resorption  are  seen  in  close  proximity.  Chronic  apical  abscess 
may  produce  a  denudation  of  the  root  end,  and  at  a  short  distance 
below  an  annular   ridge  of   hypercementosis  may  occur.      Areas  of 


HYPERCEMENTOSIS. 


507 


hypercementosis  may  be  translucent  or  decidedly  opaque,  and  some 
times  the  two  are  combined,  a  mottled  appearance  being  produced. 

If  the  growth  proximate  another  root  the  pericementum  may  resorb 
at  the  point  of  contact  and  a  deposition  of  cementum  occur  which 
firmly  unites  the  roots  in  a  union  called  concrescence.     (See  p.  222.) 


Apex  of  root  of  an  upper  bicuspid  tooth  with  irregularly  developed  cementum :  a,  a,  dentine ; 
6,  b,  pulp  canals.  The  lamellae  of  cementum  are  marked  1,  2,  3,  etc. ;  d,  d,  d,  absorption  areas 
that  have  been  refilled  with  cementum.  It  will  be  seen  that  the  apices  of  the  roots  were  orig- 
inally separate,  but  became  fused  with  the  deposit  of  the  second  lamella  of  cementum,  and  that 
in  this  the  regular  growth  began  and  was  most  pronounced.  It  has  continued  thi'ough  the 
subsequent  lamellse,  but  in  less  degree.  It  will  also  be  noticed  that  the  absorption  areas, 
d,  d,  d,  have  proceeded  from  cei-tain  lamellse.  That  between  the  roots  has  broken  through  the 
first  lamellse  and  penetrated  the  dentine,  and  has  been  filled  -with  the  deposit  of  a  second 
lamella.  Other  of  the  absorptions  have  proceeded  from  lamellse  which  can  be  readily  made 
out.  The  small  points,  e,  seem  to  have  been  filled  with  the  deposit  of  the  last  layer  of  the 
cementum,  while  others  have  one,  two,  or  more  layers  covering  them.     (Black.) 

It  has  occurred  that  a  root  filling  protruding  through  a  perforation 
has  caused  a  diffused  exostosis  of  the  alveolar  process.^  The  hyper- 
trophied  process  may  be  ivory-like  in  hardness. 

Symptoms  and  Diagnosis.  Many  cases  exist  without  active  local 
symptoms.  In  no  case  is  the  color  of  the  gum  altered  unless  other 
disease  than  hyperaemia  be  acting  as  a  cause.  In  some  cases  there  are 
symptoms  of  hypersemia  expressed  as  a  disposition  to  bite  hard  upon 
the  particular  tooth,  or  to  grind  upon  it.    A  paroxysm  of  gnawing  pain 


1  Garretson's  Oral  Clinic,  1884. 


508  DISEASES  OF  THE  PERICEMEXTUM. 

lasting  for  some  hours,  and  recurring  at  intervals,  is  also  sonaewhat 
characteristic.     The  gum  may  have  slightly  receded. 

Neuralgia,  functional  blindness,  functional  deafness,  epileptiform 
fits,  paralysis,  cardiac  neuralgia,  insanity,  and  other  related  conditions 
have  been  cured  by  the  extraction  of  hypercementosed  teeth/ 

The  treatment  of  teeth  presenting  obstinate  symptoms  of  peri- 
cementitis, apparently  due  to  moist  gangrene  of  the  pulp,  may  at  times 
be  complicated  by  unsuspected  hypercementosis. 

In  such  cases,  if  pulp  or  pericemental  complication  cannot  be  deter- 
mined, suspicion  should  point  to  hypercementosis  and  an  rc-ray  exami- 
nation be  made,  by  which  means  the  condition  may  be  positively 
determined.  As  entire  dentures  have  been  extracted,  tooth  by  tooth, 
in  a  vain  endeavor  to  cure  a  neuralgia  about  the  head,  this  means  of 
diagnosis  should  not  be  overlooked. 

Treatment.  The  treatment  for  hypercementosis  may  first  be  a 
conservative  one  if  only  slight  annoyance  be  produced  by  it. 

Counterirritation — correction  of  malocclusion,  etc. — may  be  em- 
ployed. The  symptoms  may  disappear.  If  they  do  not,  or  they 
are  severe  when  the  patient  applies,  the  tooth  should  be  completely 
extracted.  The  operation  of  amputation  of  the  root  end  might  be 
safely  tried  for  this  condition,  but  there  are  no  records  of  its  employ- 
ment as  a  means  of  cure.  The  bulbous  condition  of  the  root  end 
may  cause  extraction  to  be  difficult,  and  fracture  of  the  root  end 
may  occur.  Flagg  recommended  that  in  such  a  case  a  fissure  drill 
be  passed  about  the  circumference  of  the  root  end  to  remove  the  bony 
obstruction  to  its  passage  out  of  the  alveolus,  after  which  it  may  be 
lifted  away  with  tweezers.    Cocaine  may  be  used  as  an  obtundent. 

Extraction  for  hypercementosis  may  cause  considerable  bruising  of 
the  walls  of  the  alveolus,  followed  by  excruciating  pain  lasting  often 
for  days.  The  alveolus  may  refuse  to  granulate  and  a  septic  condition 
result.  The  pain  has  at  times  been  relieved  by  the  injection  of  a 
2  per  cent,  solution  of  cocaine  into  the  gum  on  either  side  of  the  alveolus, 
after  which  the  surfaces  of  the  alveolar  walls  should  be  sterilized  and 
burred  away  until  tissue  capable  of  granulation  is  reached. 

The  alveolus  should  then  be  irrigated  and  a  clot  invited  by  causing 
a  slight  hemorrhage.     (See  p.  492.) 

1  Brubaker,  American  System  of  Dentistry. 


ANKYLOSIS.  509 

(ANKYLOSIS)  SYNOSTOSIS. 

By  this  is  meant  the  union  of  bone  and  cementum,  a  condition 
analogous  to  ankylosis  of  bone. 

Hopewell-Smith^  has  described  five  cases,  of  which  he  offers  the 
following  explanation:  (1)  inflammation  occurs  and  the  membrane  is 
changed  into  granulation  tissue;  (2)  the  cellular  elements  destroy 
portions  of  the  bone  and  excavate  the  cementum;  (3)  the  mass  of 
granulation  tissue  is  then  ossified,  joining  the  bone  and  cementum  in 
a  firm  union. 

Fig.  458. 


Vertical  section  of  a  human  tooth  ankylosed  to  the  jaw:  B,  root;  B,  bone  of  jaw.  The  abso- 
lute continuity  of  the  two  hard  tissues  is  strikingly  shown.  From  the  coUection  of  the  late 
Storer  Bennett. i     (Hopewell-Smith.) 

RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH. 

By  resorption  of  the  roots  of  permanent  teeth  is  meant  the  gradual 
removal  of  the  cementum  and  dentine  of  permanent  roots  by  phago- 
cytic cells  existing  in  the  adjacent  soft  tissue  (osteoclasts). 

Causes.  The  proximate  cause  is  probably  in  all  cases  a  degree  of 
irritation  greater  than  that  required  to  produce  hypercementosis. 
Talbot's  demonstrations  upon  interstitial  gingivitis,  a  term  meant  to 

1  Histology  and  Pathohistology  of  the  Teeth. 

2  Transactions  of  the  Odontological  Society  of  Great  Britam. 


510  DISEASES  OF  THE  PERICEMEXTUM. 

include  interstitial  pericementitis,  show  that  it  is  a  frequent  cause  of 
both  root  and  alveolar  resorption.     (See  Interstitial  Gingivitis.) 

The  disease  has  been  discussed  by  other  writers  as  a  result  of 
"Rarefying  Pericementitis." 

Chronic  apical  abscess  seems  to  be  a  frequent  cause.  Although 
theoretically  the  alkaline  pus  formed  should  neutralize  acid  formation, 
the  fact  of  resorption  remains  and  is  probably  explained  upon  the 
ground  that  it  is  produced  by  the  granulation  tissue  formed  about 
the  root  apex  during  periods  of  lessened  pus  formation. 

Protruding  root  fillings  or  broaches  are  common  causes  (Fig.  457). 
Plantations  are  frequently  followed  by  it.  Looseness  of  a  tooth  with 
the  resultant  excess  of  movement  excites  interstitial  gingivitis.  Partial 
luxation  as  the  result  of  a  blow  or  fall  produces  the  same  result,  the 

Fig.  457.  Fig.  458. 


Apical  abscess  and   resorption,  iiroduced  Deciduous  cuspid  crowned,  mistaken  for 

by  a  protruding  broach.  permanent    cuspid   which    lay  in    jaw  and 

caused  resorption  of  root  of  permanent  lat- 
eral.    (Skiagraph  by  Price.) 

pericementum  becoming  thickened,  the  tooth  loosened  and  extruded, 
and  malocclusion,  which  is  also  a  cause,  being  induced. 

A  toothpick  broken  off  in  the  gum  tissue  has  produced  resorption 
at  the  neck  of  the  root. 

The  descent  of  a  supernumerary  or  impacted  tooth  upon  a  permanent 
root  has  caused  resorption,  exposing  the  pulp  of  the  resorbed  root,  and 
producing  pulp  reactions.  This  may  be  quite  extensive  before  violent 
symptoms  occur  (Fig.  458). 

Calculus  beneath  the  gum  margin  has  produced  resorption.  In  one 
case  noted  four  lower  incisors  presented  the  characteristic  bays  at  a 
point  one-eighth  inch  below  the  gum  line. 

Some  of  the  cases  exhibit  no  tangible  cause;  the  root  resorbs  appar- 
ently as  the  result  of  a  peculiar  reaction  upon  the  part  of  the  tissues 
of  the  individual,  who  may  lose  many  teeth  by  this  process — i.  e.,  a 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH.       51 1 

dyscrasia  exists.  The  teeth  may  be  non-carious  and  the  pulps  vital. 
In  some  of  these  cases  neurasthenia  or  a  uric  acid  diathesis  seems  to 
have  some  association  with  the  condition. 

Pathology  and  Morbid  Anatomy.  Both  resorption  of  cementum  and 
its  redeposition  occur  in  teeth  as  physiological  processes;  at  some 
aspect  of  the  cementum  the  tissue  becomes  hollowed  out,  and  later 
filled  in  by  new  cementum.  Resorption  of  tissue  throughout  the  body 
is  accomplished  by  means  of  multinucleated  cells  (giant  cells,  osteo- 
clasts). At  some  part  to  be  physiologically  resorbed  these  cells  make 
their  appearance  in  contact  with  the  tissue  to  be  removed,  and  it 
gradually  disappears,  the  layer  of  multinucleated  cells  constantly 
occupying  the  excavated  territory. 

If  a  foreign  (aseptic)  body  be  introduced  into  living  tissues,  it 
becomes  surrounded  by  these  cells,  which  in  some  cases  effect  its 
removal;  in  others,  failing  to  remove  the  foreign  body,  connective 
tissue  forms  about  it  and  encysts  it;  encystment  may  occur  after 
partial  removal  by  giant  cells. 

The  resorption  may  be  of  any  extent,  from  a  slight  spicular  rough- 
ness of  the  apex  of  the  root  to  almost  complete  removal  of  the  root. 

Perforation  of  the  root  from  side  to  side  may 
occur,  of  course,  involving  the  pulp  canal  and, 
if  the  pulp  be  alive,  obscure  reactions  upon  its 
part  may  occur. 

An  area  of  marked  resorption  may  occur  at  a 
point  just  beneath  the  gum  margin  and  upon 
any  aspect  of  the  tooth.  In  this  situation  it  may 
simulate  a  cavity  of  decay  beneath  the  gum.     It 

.,^  .,1  1       •,    T        1    J.      J.I,  J        Idiopathic  resorption  of 

occurs  upon  either  vital  or  devitanzed  teetn  and  permanent  root.  The  bay 
may  expose  the  pulp  or   the   root-canal   filling  upon  the  side  exposed  the 

/  ^  .  ,.  pulp  and    perforated   the 

(Fig.  459).      After   plantations    peculiar  resorp-  root  as  shown,  crater-uke 

tions  over  even  the  entire  root  may  occur.         ^     ZZ^^^ZUZ^. 

It  is  probable  that  in  plantations  the  root  is  taiized  on  account  of  per- 

,     ,  •        (>         •  1        1  'IJ     •  sistent  pain  and  the  tooth 

regarded  as  an  aseptic  foreign  body;  mud  m-  later  extracted. 
flammation  occurs,  subsides,  and  giant  multi- 
nucleated cells  attack  the  tooth  root  and  endeavor  to  remove  it  by 
solution;  this  they  accomplish  in  part  in  spots;  then  a  tolerance  is 
established  and  connective  tissue  organizes  about  the  roots;  later  more 
complete  regeneration  is  represented  in  the  formation  of  bone;  a  con- 
dition of  bony  fixation  is  established,  evidenced  by  the  clear-ringing 
note  elicited  upon  tapping  the  planted  tooth. 


512  DISEASES  OF  THE  PERICEMEXTUM. 

The  inflammatory  reaction  and  resorption  is  least  when  replantation 
is  practised,  but  may  at  times  be  pronounced  in  even  those  cases.  If 
the  socket  of  a  tooth  extracted  for  resorption  be  examined,  a  mass  of 
soft  tissue  will  be  found  occupying  the  locations  corresponding  to  the 
areas  of  resorption  (Fig.  460).  These  soft  masses  correspond  to 
granulation  tissue.  No  acid  reaction  can  be  detected  with  litmus  paper, 
but,  nevertheless,  it  is  probable  that  the  cells  producing  resorption 
excrete  an  acid  capable  of  dissolving  the  tissue. 

There  is  some  evidence  of  this  in  cases  of  enamel  resorption  occur- 
ring upon  the  crowns  of  impacted  teeth  which  have  never  been  in 
relation  with  the  oral  fluids,  and  about  which  there  is  no  evidence  of 
caries  in  the  areas  of  dentine  resorption  also  present.  In  the  fortunate 
.specimens  of  these  cases  a  superficial  decalcification  of  the  enamel 
surface  may  be  seen  which  can  only  occur  as  the  result  of  acid  action. 

Fig.  ^60.  Fig.  461. 


Diagram  of  a  case  of  root  resorption  after 
secondary  dentine  had  formed;  SD,  secondary 

dentine;     AR,   area    undergoing    resorption; 

Resorption  of  distal  rout  ot  u  thst  molar.  peculiar   central   spire  of   secondary  dentine. 

(Skiagraph  by  Custer.)  Specimen  in  possession  of  Dr.  A.  P.  Fellows. 

Symptoms  and  Diagnosis.  The  tooth  may  present  symptoms  of 
non-septic  pericementitis,  and  may  be  loosened  in  advanced  cases. 
In  the  early  stages  no  looseness  may  be  observed  until  a  strain  suddenly 
applied  causes  a  luxation;  thereafter  the  tooth  progressively  loosens. 

The  condition  may  be  discovered  by  accident:  evidences  of  mild 
pericementitis  appear,  and  the  pulp  canal  is  opened  to  search  for  a 
cause.  The  pulp  may  be  found  alive;  if  alive,  and  it  is  killed,  or  if  it 
is  found  dead,  broaches  pass  suddenly  into  the  mass  of  soft  tissue 
underlying  the  root.  The  progressive  loosening  of  the  tooth,  with 
its  peculiar  movement,  is  about  the  only  constant  symptom  of  the 
condition. 

In  cases  of  live  pulp  this  organ  may  be  hypersemic,  so  that  increased 
response  to  heat  or  cold  is  felt;  this,  taken  in  connection  with  the 
tenderness  upon  percussion  which  can  usually  be  elicited,  and  with 
the  pecuHar  loosening  of  the  tooth,  is  a  diagnostic  guide. 


OVERUSE  OF  TEETH.  513 

Flagg^  states  that  reflex  neuralgias  occur  in  this  condition,  but  that 
the  most  constant  indication  noted  by  him  was  a  sense  of  discomfort 
about  the  jaws,  vaguely  associated  with  some  one  tooth.  The  patient 
is  convinced  that  if  the  tooth  were  removed  relief  would  follow.  In 
the  absence  of  the  loosening,  which  may  not  occur  until  the  root  is 
nearly  gone,  the  resorption  is  most  commonly  discovered  by  entering 
the  pulp  canal  and  finding  its  length  much  shortened.  In  some  cases 
the  resorption  may  be  found  near  the  gum  margin  and  simulating  a 
cavity  of  decay,  from  which  it  may  readily  be  diagnosed  by  its  appear- 
ance when  exposed  by  packing  the  gum  away.  Such  cases  appear 
to  accompany  a  marginal  gum  resorption. 

The  rc-ray  should  exhibit  the  condition  with  sufficient  clearness  to 
furnish  an  absolute  diagnosis. 

If  a  direct  diagnosis  can  be  made  the  tooth  should  be  extracted, 
except  in  the  cases  near  the  gum  margin,  which  may  be  filled  usually 
with  plastic  fillings.  If  a  diagnosis  be  not  possible,  probable  causes  of 
irritation  should  be  sought  for  and  removed  and  the  non-septic  peri- 
cementitis treated  as  indicated.     (See  p.  502.) 

Failing  a  cure  the  tooth  is  to  be  removed,  when  a  post  hoc  diagnosis 
may  be  made.  In  view  of  the  availability  of  the  a;-rays  this  involves 
an  unnecessary  endurance  and  loss  of  time. 

DEGENERATION  OF  THE  PERICEMENTUM. 

Strictly  speaking,  the  overuse,  abuse,  and  disuse  of  the  teeth  are 
causes  which  produce  a  general  hypersemia  or  inflammation  of  the 
pericementum  (interstitial  gingivitis).  These  either  render  it  liable 
to  the  degenerations  and  resorptions  which  accompany  continued 
hypersemia  or  inflammation,  or  act  as  a  predisposing  cause  to  local 
infection  by  oral  organisms,  beginning  their  action  at  the  gum  margin, 
and  sooner  or  later  producing  a  purulent  or  non-purulent  liquefaction 
of  the  gingival  portion  of  the  pericementum  (pyorrhoea  alveolaris). 

In  view  of  applied  therapeutics  it  is  well  to  consider  these  causes 
separately. 

OVERUSE  OF  TEETH. 

By  overuse  of  a  tooth  is  meant  such  a  variety  of  occlusion  that  the 
tooth  receives  a  greater  stress  than  its  neighbors,  or  than  it  is  designed 
to  bear.  The  stress  may  be  received  in  the  normal  direction,  but  be 
excessive  in  amount.    The  most  prominent  cause  of  this  condition  is 

1  Lectures  on  Dental  Therapeutics. 
33 


514  DISEASES  OF  THE  PERICEMENTUM. 

the  loss  of  one  or  more  other  teeth,  permitting  undue  stress  to  fall  upon 
the  neighboring  teeth,  or,  in  some  cases,  on  far-distant  teeth.  Too 
prominent  artificial  crowns,  particularly  those  of  the  all-gold  t}^e, 
cause  a  general  increase  of  stress  upon  the  pericementum.  Enormous 
overfull  contour  fillings  may  establish  a  similar  condition.  When  but 
few  isolated  teeth  remain  in  one  denture  and  have  antagonists,  the 
teeth  are  certain  to  be  overworked.  Isolated  and  other  teeth,  to  which 
are  attached  clasps  of  artificial  dentures,  are  in  the  majority  of  cases 
being  constantly  overstrained. 

Pathology.  Like  any  other  functional  part  which  is  overworked, 
the  pericementum  is  first  stimulated,  causing  the  vessels  to  dilate. 
Soon  evidences  of  overwork  appear  in  a  passive  dilatation  of  the  peri- 
cemental vessels,  and  atonic  hypersemia  is  established.  The  condition 
passes  into  one  of  irritation  and  interstitial  gingivitis;  the  tooth  projects, 
and  is  loosened;  the  overlying  gum  deepens  in  color,  and  evidences  of 
venous  encrorgement  are  common.  The  result  of  the  condition  is  a 
softening  and  degeneration  of  the  substance  of  the  pericementum;  the 
alveolar  wall  is  involved  in  the  degeneration,  and  it  melts  down — is 
resorbed  to  a  greater  or  less  extent.  At  any  stage  of  the  disturbance 
infection  may  occur,  and  the  degeneration  and  destruction  of  the  peri- 
cementum be  hastened  by  suppuration  or  other  secondary  degen- 
erations. 

The  s}Tnptoms,  diagnosis,  and  clinical  history  are  involved  in  the 
description.  The  prognosis  is  the  inevitable  loss  of  the  tooth  if  the 
causes  be  not  removed,  in  which  event  the  prognosis  is  governed  by 
the  extent  to  which  the  degeneration  has  proceeded.  (See  Interstitial 
Gingivitis.) 

Treatment.  The  treatment  is  the  removal  of  the  causes  and  pro- 
curing surgical  rest  until  the  injured  pericementum  has  recovered. 
The  insertion  of  carefully  made  artificial  dentures  is  indicated  in  those 
cases  of  scattered  natural  teeth  having  spaces  between  them.  The 
prosthetic  appliance  must  not  be  attached  to  these  teeth,  nor  in  its 
movements  should  it  bear  against  them.  No  attem'pt  is  made,  however, 
to  cause  the  artificial  teeth  to  strike  before  the  natural  teeth  in  the 
hope  of  giving  surgical  rest  to  these  organs.  Such  attempts  always 
result  in  failure,  as  they  cause  injuries  to  the  tissues  upon  which  the 
plate  and  teeth  rest,  which  are  more  severe  than  the  pericemental 
disturbance. 

Properly  adjusted  bridge-work  frequently  does  good  service  in  these 
cases,  pro\dded  the  overoccluding  tooth  or  teeth  be  first  dressed  down 


MALOCCLUSION  OF  THE  TEETH.  51 5 

short  of  occlusion  and  are  given  a  period  of  rest  until  the  peri- 
cementum recovers.  The  bridge,  if  carefully  planned,  may  be  made 
to  direct  and  control  the  stress  received  by  the  injured  teeth. 

Improperly  occluding  artificial  crowns  should  have  this  fault 
corrected  by  removing  the  excess  of  material  or  by  setting  properly 
made  crowns. 

Overfull  fillings  should  be  reduced  to  correct  proportions  and 
shape. 

Teeth  which  are  being  strained  by  clasps  should  have  the  latter 
removed.  If  necessary,  a  new  appliance  should  be  made  on  which 
clasps  are  either  omitted  or  are  properly  designed  for  other  teeth. 

Surgical  rest  is  the  only  hope  of  saving  the  tooth. 

MALOCCLUSION  OF  THE  TEETH. 

Each  tooth  of  a  denture  is  not  only  designed  to  receive  a  definite 
amount  of  force,  but  to  receive  it  in  a  particular  direction  or  directions; 
any  excess  of  this  force,  or  alteration  of  its  direction,  is  followed  by 
abnormal  stimulation  of  the  pericementum  and  by  its  overstraining. 
(See  Chapter  VIII.)  The  effects  following  a  general  increase  of  stress 
have  been  .considered  under  the  previous  heading.  By  malocclusion 
is  here  meant  the  constant  reception  of  stress  by  the  pericementum 
in  directions  to  which  it  is  quite  unaccustomed,  or  are  not  in  accord- 
ance with  the  anatomical  design  of  the  tooth.  It  is  a  peculiar  form  of 
overuse. 

Causes.  Original  malpositions  of  the  teeth  may  cause  their  faulty 
occlusion.  The  most  prolific  source  of  the  condition  is,  however, 
altered  occlusion  due  to  those  changes  of  position  of  the  teeth  M'hich 
follow  upon  the  loss  of  adjoining  teeth. 

Artificial  crowns  which  do  not  occlude  in  correspondence  with  the 
other  teeth  are  a  common  cause.  Improperly  formed  fillings  are 
another  cause. 

The  shifting  of  positions  of  the  teeth,  in  consequence  of  pathological 
changes  occurring  in  or  about  the  pericementum,  cause  the  crowns  of 
teeth  to  occlude  improperly. 

Pathology.  The  conditions  established  are  those  of  overuse  in  a 
direction  other  than  direct.  A  typical  example  of  this  condition  is  that 
of  a  lower  second  molar  which  has  gradually  tilted  forward  in  conse- 
quence of  the  loss  of  the  first  molar;  or  a  central  incisor  which  has 
altered  its  position  in  consequence  of  secondary  formations  in  or  about 


516  DISEASES  OF  THE  PERICEMENTUM. 

the  pericementum,  a  common  precursor  of  phagedenic  pericementitis. 
Some  portion  of  the  tooth,  an  edge,  which  before  did  not  occlude  with 
an  antaeonizins  tooth,  is  brought  into  occlusion;  if  the  occlusion  be 
not  unduly  forcible,  no  immediate  degenerative  changes  are  evident. 
If  the  occlusion  be  excessive,  the  pericementum  is  not  uniformly- 
affected,  but  the  greatest  stress  is  brought  to  bear  upon  some  lateral 
aspect  of  the  structure.  It  responds  in  the  degree  of  the  overwork, 
and  degenerative  changes  occur  which,  if  the  active  causes  be  not 
removed,  gradually  spread  to  other  portions  of  the  pericementum,  and 
the  phenomena  noted  in  connection  with  overuse  occur,  but  are  not 
so  general  in  distribution.  The  tooth  becomes  more  movable  in  one 
or  more  directions — i.  e.,  is  loosened;  it  may  develop  some  degree  of 
tenderness  upon  percussion,  and  the  gum  color  toward  the  affected 
side  deepens,  although  it  may  remain  normal  in  other  parts.  As  in 
the  previous  cases,  infection  may — indeed,  is  likely  to— occur.  In 
some  cases  the  pericementum  may  degenerate  and  be  destroyed  about 
one  root  of  a  multirooted  tooth,  and  remain  about  the  other.  It  is 
to  be  remembered  that  a  less  degree  of  irritation  may  produce  hyper- 
cementosis. 

Diagnosis  and  Treatment.  In  all  malposed  teeth  a  careful  examina- 
tion should  be  made  of  their  mode  of  occlusion.  If  the  tooth  exhibit 
tenderness  and  looseness,  malocclusion  is  almost  a  certainty;  it  only 
remains  to  determine  its  direction. 

The  spots  of  faulty  occlusion  may  be  determined  by  placing  a  strip 
of  carbon  paper  (articulating  paper)  over  the  tips  of  the  antagonizing 
teeth  and  having  the  patient  bite;  the  spots  of  contact  should  then 
be  ground  away  until  the  tooth  is  slightly  short  of  direct  occlusion. 
Fresh  strips  of  paper  are  used,  and  the  jaws  moved  laterally,  as  in 
mastication,  to  note  other  points  of  contact;  these  should  also  be 
ground  away. 

Prognosis.  If  the  condition  be  not  corrected  every  time  occasion 
requires,  the  degeneration  progresses  until  the  tooth  is  lost. 

If  marginal  infection  has  occurred,  purulent  or  non-purulent  marginal 
pericemental  liquefaction  (pyorrhoea  alveolaris)  may  have  to  be  con- 
sidered. 

DISUSE  OF  TEETH. 

Definition.  By  disuse  of  teeth  is  meant  a  degree  of  usage  less  than 
the  amount,  the  forms,  and  structure  of  the  teeth  and  contiguous  parts 
fit  them  for.    The  disuse  may  be  absolute  or  relative;  teeth  may  not 


DISUSE  OF  TEETH.  5I7 

occlude  at  all,  owing  to  the  loss  of  antagonists  or  to  extremely  irregular 
positions. 

Partial  Disuse.  Causes  and  Pathology.  If  soft  food  be  used  instead 
of  that  requiring  vigorous  mastication,  or  if  one  tooth  of  a  side  be 
diseased  so  that  that  side  of  the  mouth  is  unused  in  mastication,  or  if 
one  of  the  antagonists  of  a  tooth  be  lost,  the  pericementi  of  the  teeth 
involved  do  not  receive  their  proper  amount  of  exercise  and  a  degree 
of  atony  ensues. 

This  partial  disuse  has  a  more  distinct  relation  to  the  health  of  the 
gum  margin,  which  does  not  receive  a  normal  amount  of  friction  from 
mastication,  and  if  this  be  not  offset  in  part  by  the  use  of  the  tooth- 
brush, atony,  followed  by  passive  hypersemia  of  the  gum  margin, 
ensues. 

Infection  and  the  formation  of  calculus  increase  the  irritation  to  a 
marginal  gum  inflammation  which  is  liable  to  run  into  a  pyorrhoea 
alveolaris.    This  is  the  real  significance  of  disuse  as  a  cause. 

Diagnosis  and  Prognosis.  A  diagnosis  of  disuse  (relative)  is  usually 
made  out  by  inquiring  as  to  the  food  habit  of  individuals.  It  is 
excessively  common  in  civilized  communities,  particularly  among  the 
well-to-do,  and  is  of  almost  constant  occurrence  in  gourmands. 

Treatment.  Patients  should  have  pointed  out  to  them  the  results 
of  insufficient  mastication,  together  with  the  evils  of  faulty  oral  hygiene. 
Every  effort  should  be  made,  by  the  use  of  constant  prophylactic 
measures,  to  forestall  the  occurrence  of  pyorrhoea  alveolaris.  This 
and  similar  conditions  are  particularly  to  be  feared  in  the  degenerative 
periods  of  early  and  late  middle  age.  It  is  between  the  ages  of  thirty 
and  fifty  years  that  ill-consequences  are  most  to  be  feared  from  acquired 
debility  of  the  pericementum. 

Absolute  Disuse.  Teeth  which  perform  no  work  directly  in  masti- 
cation, or  indirectly  by  serving  as  abutments  for  a  bridge-piece,  may 
be  said  to  be  in  a  condition  of  absolute  disuse. 

Results.  A  tooth  or  root  whose  pericementum  receives  no  stimulus 
becomes  relatively  a  foreign  body  to  the  organism.  It  is  a  useless  part, 
and  the  body  attempts  to  cast  it  out.  Perhaps  these  phases  are  insuf- 
ficiently exact;  however,  a  disused  tooth  is  lost  through  a  series  of 
pathological  changes.  Teeth  which  perform  no  work  may  be  retained 
in  the  mouths  of  young  adults  for  long  periods  without  marked 
changes  occurring  in  their  vital  connections,  but  during  the  degen- 
erative period  of  life  they  are  usually  lost  with  a  degree  of  rapidity 
differing  in  individuals. 


518  DISEASES  OF  THE  PERICEMENTUM. 

The  pericemental  condition  of  passive  hyperaemia  following  upon 
relative  disuse  of  the  teeth  has  been  described ;  the  condition  following 
upon  absolute  disuse  differs  in  that  the  pericementum  receives  no 
exercise  whatever.  The  clinical  history  of  these  cases  is  that  of  a 
progressive  extrusion  of  the  tooth;  it  projects  beyond  its  fellows  in 
increasing  degree.  The  borders  of  the  alveolar  process  recede,  but 
usually  to  less  extent  than  the  tooth  protrudes  or  is  extruded.  The 
tooth  becomes  progressively  looser,  until  in  its  latest  stages  a  portion, 
which  may  be  one-half  of  its  root  leng'th,  is  attached  to  the  jaw  through 
the  medium  of  a  mass  of  soft  tissue  alone;  all  true  alveolar  connection 
has  disappeared.    After  extraction  or  complete  extrusion,  the  root  of 


Absolute  disuse  and  elongation  of  an  upper  and  a  lower  molar ;  partial  disuse  of  bicuspid ; 
small  abscess  cavity  in  the  bone  about  a  root.    (Philadelphia  Dental  College  Museum.) 

the  tooth  is  seen  to  be  devoid  of  pericementum  except  at  the  apex  of 
the  root.  The  alveolar  process  has  undergone  limited  atrophy,  although 
in  some  cases  its  outer  walls  may  be  thickened. 

Pathology.  The  passive  hypersemia  has  apparently  led  to  swelling 
and  degeneration,  with  subsequent  atrophy  of  the  pericementum,  and- 
the  normal  atrophic  changes  which  occur  in  the  alveolar  process  have 
become  hastened  and  quickened.  These  cases  frequently  become  com- 
plicated by  infections,  when  the  tooth  loosening  becomes  pronounced. 
The  pulp  vessels  are  cut  off  and  the  dead  pulp  tissue  furnishes  a  soil 
for  micro-organisms,  whose  poisons  hasten  degeneration  of  the  tissues 
in  the  abnormal  alveolus.  Suppuration  may  occur — i.  e.,  abscess  form. 
Through  this  process  the  jaws  cast  out  crownless  roots;  in  these  the 


FIBROID  DEGENERATION  OF  THE  PERICEMENTUM.        519; 

local  alveolar  atrophy  may  be  complete  before  there  is  any  external 
evidence  of  it. 

The  danger  of  marginal  infection  is  always  great  in  these  cases. 
Some  degree  of  infection,  no  doubt,  exists  in  all  of  them,  which  serves 
to  explain  the  increased  rapidity  of  the  degenerations. 

Prognosis.  If  teeth  can  be  directly  or  indirectly  brought  into  use,, 
so  that  their  pericementi  receive  exercise,  the  cases  may  recover,  pro- 
vided the  atrophic  changes  are  not  very  pronounced;  in  which  event 
the  atrophy  proceeds,  although  more  slowly.  Teeth  crowned  or  made 
abutments  for  bridges,  after  degenerative  changes  have  become  estab- 
lished—i.  e.,  when  the  normal  pericementum  has  been  replaced  by 
a  thickened  mass  of  partially  organized  connective  tissue — usually 
become  progressively  looser;  the  alveolar  atrophy  proceeds  until  all 
attachment  is  lost. 

If  this  is  utilized  early,  the  teeth  may  be  saved.  The  results  are 
better  if  the  teeth  or  roots  be  utilized  before  the  age  of  thirty  than 
at  later  ages. 

Treatment.  The  treatment,  as  might  be  inferred  from  the  foregoing 
statements,  consists  in  bringing  the  teeth  into  use,  if  the  degeneration 
have  not  proceeded  too  far.  Later,  extraction  is  inevitable.  The 
operation,  when  determined  upon,  should  not  be  delayed,  for  not  only 
are  bacterial  growths  invited  about  the  loosened  tooth,  but  the  soft 
tissues  are  frequently  increased  in  volume,  and  if  extraction  be  delayed 
until  complete  local  atrophy  of  the  alveolar  walls  has  taken  place,  a 
soft  and  spongy  mass  remains,  which  interferes  with  the  comfortable 
wearing  of  prosthetic  appliances  in  the  future. 


FIBROID  DEGENERATION  OF  THE  PERICEMENTUM. 

Fibroid  degeneration  of  the  pericementum  is  a  senile  atrophic  change 
occurring  in  teeth,  the  pericementi  of  which  have  run  a  healthy  life 
course,  but  finally  have  become  subject  to  senile  marantic  constitutional 
changes  of  not  clear  nature.  The  condition  thus  first  defined  by 
Hopewell-Smith^  is  further  described  as  found  in  that  class  of 
teeth  of  the  aged  which  have  resorbed  alveolar  margins  and  exposed 
cementum,  but  not  necessarily  subject  to  pyorrhoea  alveolaris;  though 
traumatic  pericementitis  may  be  present.  In  some  cases  the  teeth  may 
be  firm. 

1  Dental  Cosmos,  1904. 


520 


DISEASES  OF  THE  PERICEMENTUM. 


Pathohistology.  The  chief  characteristics  are  an  increase  in  size 
of  the  fibres  of  the  pericementum,  the  loss  of  their  nuclei,  and  their 
generally  structureless  character,  and  their  arrangement  in  prominent 
bundles  about  large  spaces  (areolae).     (See  Fig.  463.) 

The  fibres  are  firmly  implanted  in  both  bone  and  cementum.  The 
cementum  does  not  become  hyperplastic  (hypercementosed),  but  the 
bone  becomes  osteoporous  and  the  Haversian  canals  contain  a  shrunken 
fibroid  tissue  resembling  that  in  the  pericementum  (Fig.  464). 

Fig.  463. 


J  \^ 


Fibroid  degeneration  of  the  pericementum:   C,  cementum;  A,  alveolus;  F,  fibres  with  decrepit 
nuclei.     Transverse  section.     (Hopewell-Smith.) 


The  gum  tissue  in  the  vicinity  also  undergoes  retrogressive  changes 
in  sympathy,  becomes  less  vascular  and  more  fibroid. 

The  condition  may  persist  without  inflammatory  or  suppurative 
changes,  though  it  may  act  as  a  cause  of  obscure  neuralgia  or  as  a 
predisposing  cause  to  pyorrhoea  alveolaris. 

Hopewell-Smith  points  out  that  the  areolar  spaces  may  admit  micro- 
organisms to  deep  parts,  thus  predisposing  to  antral  disease  or  possibly 
osteomyelitis. 


ACCIDENTS  TO  TEETH. 

Fig.  464. 


521 


—  H 


—  M 


Fibroid  degeneration  of  the  pericementum:  C,  cementum;  M,  degenerated  pericementum; 
A,  alveolus;  H,  enlarged  (osteoporous)  Haversian  canals.  Transverse  section.  (Hopewell- 
Smith.) 

ACCIDENTS  TO  TEETH. 

Apart  from  fracture  of  the  teeth  by  accidents,  several  interesting 
accidental  conditions  involving  therapeutics  require  consideration. 

Teeth  Driven  into  Alveolar  Process.  Blows,  falls,  etc.,  have  occa- 
sionally caused  teeth  to  be  driven  forcibly  into  the  jaw.  The  condition 
may  be  complicated  by  fracture,  in  which  case  the  judgment  of  the 
operator  must  be  exercised.  If  the  tooth  be  not  fractured  it  may  be 
drawn  down  with  forceps  and  ligated  in  place  until  firm.  If  evidence 
of  pulp  death  be  noted  by  subsequent  test,  or  apical  pericemental 
inflammation,  the  pulp  should  be  removed. 

Luxation  or  Partial  Dislocation  by  Accident.  Teeth  may  be 
partially  knocked  out  and  driven  either  hngually  or  buccally.  The 
pulp  connections  will  be  ruptured,  as  a  rule,  but  after  asepsis  of  the 
parts  by  means  of  antiseptic  sprays  the  teeth  may  be  pressed  into  place, 
and  if  ligated  or  splinted  may  again  become  firm  by  deposition 
of  bone  about  them.  The  pulps  nearly  always  give  evidence  of  death; 
so  that  the  pulps  should  be  replaced  with  canal  fillings. 


522  DISEASES  OF  THE  PERICEMEXTUM. 

Occasionally  evidences  of  reattachment  of  pulp  have  been  recorded/ 
even  after  total  displacement.  If  the  accident  result  in  elongation  of 
the  tooth  with  production  of  a  chronically  spongy  pericementum, 
the  operation  of  replantation  should  be  performed. 

Total  Dislocation  of  Teeth  by  Accident.  If  the  accident  result  in 
total  displacement  from  the  mouth  the  tooth  or  teeth  may  be  prepared 
as  for  replantation  (see  p.  488),  and  under  aseptic  precautions 
replanted  in  their  alveoli.  If  held  by  ligatures  or  splints  they  will 
usually  become  firm. 

Attachment  of  Teeth.  Two  or  more  teeth  may  be  attached  by  the 
intervening  alveolar  process,  fracture  of  which  may  cause  both  teeth 
to  be  removed  in  extraction.  In  a  few  cases  of  loose  deciduous  teeth 
the  gum  has  been  sufficient  attachment  to  cause  the  removal  of  two 
teeth  at  once. 

In  some  cases  the  tough,  fibrous  nature  of  the  pericementum  causes 
the  alveolar  bone  fractured  by  the  leverage  upon  it  to  remain  attached 
to  the  tooth. 

Fracture  of  the  Alveolar  Process.  Slight  fractures  of  the  alveolar 
plate  are  of  little  consequence  as  a  rule.  In  some  cases  one  plate  may 
be  fractured,  and,  unless  removed  with  the  tooth,  may  usually  be 
pressed  back  into  place.  Reunion  may  be  looked  for  if  asepsis  be 
maintained.  Fractures  of  the  alveolar  process  from  blows,  kicks,  etc., 
upon  the  jaw  may  become  septic  and  sequestra  may  form,  necessitating 
removal  of  both  bone  and  teeth.  Such  fractures  should  have  immediate 
attention. 

Hemorrhage  following  Extraction.  Even  in  the  absence  of 
haemopliilia  postextraction  hemorrhage  may  be  somewhat  severe,  and 
is  well  controlled  by  a  httle  tannic  acid  or  powdered  alum  upon  a 
pellet  of  cotton,  or  nosophen  gauze  w^et  with  phenol-sodique. 

If  necessary  a  linen  compress  should  be  placed  over  it  and  a  Barton 
or  Garretson  bandage  applied.  The  internal  use  of  calcium  chloride 
or  other  haemostatic  is  indicated  if  the  bleeding  be  continued. 

1  Kirk  and  W.  Truemaii. 


SECTION   YI. 

PERICEMENTAL   DISEASES   BEGINNING  AT 
THE  GUM  MARGIN. 


CHAPTER  XXIII. 

Nearly  all  the  degenerations  of  the  pericementum  which  begin 
at  the  gum  margin  are  sooner  or  later  accompanied  by  suppurative 
processes,  which  give  a  generic  name  to  these  conditions,  viz.,  pyor- 
rhoea alveolaris.  Under  this  head  dental  writers  have  included  several 
disease  processes  which  should  be  clearly  differentiated  from  one 
another.  In  general  terms  these  diseases  are  characterized  by  an 
inflammation  originating  about  the  gum  margin,  and  followed  by  a 
progressive  degeneration  and  atrophy  of  the  pericementum  and  of  the 
alveolar  walls.  In  the  areas  of  pericemental  atrophy  and  death  pro- 
gressive deposits  of  calculi  take  place,  and  infection  of  the  disease 
territory  by  pyogenic  organisms  is  the  rule.  Their  characteristics, 
therefore,  are  loss  of  pericementum  in  any  direction,  forming  pockets 
in  which  calculi  deposit,  and  from  which  pus  exudes  or  may  be  pressed. 
The  primary  cause  of  the  atrophy,  pericemental  necrosis,  calculi,  and 
infection  are  so  clearly  associated  with  a  primary  affection  of  the 
gums  about  the  necks  of  the  teeth,  that  a  critical  examination  of  the 
causes,  clinical  history,  and  pathology  of  inflammation  of  the  gum 
margin  is  a  necessary  preHminary  to  the  study  of  the  later  degen- 
erations. 

GINGIVITIS. 

By  gingivitis  is  meant  an  inflammation  of  the  gum.  When  distinctly 
confined  to  the  gum  margin  it  may  be  designated  as  marginal  gingi- 
vitis. When  the  inflammation  has  reached  the  deeper  connective 
tissues  of  the  gum  and  pericementum  it  has  been  called  interstitial 
gingivitis  (Talbot). 


524    PERICEMENTAL  DISEASES  BEGINXIXG  A  T  THE  GUM  MARGIN. 

MARGINAL  GINGIVITIS. 

Definition.  By  marginal  gingivitis  is  meant  an  inflammation  con- 
fined to  the  margins  of  the  gums  about  the  necks  of  the  teeth. 

Causes.  The  causes  of  marginal  gingivitis  are  local  and  general, 
which  may  be  subdivided  into  predisposing  and  exciting.  Both  local 
and  general  causes  may  be  in  action  at  the  same  time. 

Local  Causes.  Marginal  gingivitis  may  be  excited  by  the  pres- 
ence of  food  masses  or  unremoved  collections  about  the  necks  of  teeth, 
their  fermentation  liberating  chemical  products  more  or  less  irritating. 

^Nliller^  has  shown  that  the  materies  alba  about  the  necks  of  teeth 
may  have  either  an  alkaline  or  acid  reaction  and  the  gums  be  in- 
flamed. 

Bacterial  plaques  not  unlike  those  producing  dental  caries  have 
been  shown  by  Miller^  to  be  formed  upon  many  surfaces  of  the  teeth 
even  when  no  ill  results  are  notable.  In  practice  staining  the  teeth 
with  tincture  of  iodine  will  readily  demonstrate  the  presence  of  such 
bacterial  films.  Under  favoring  circumstances  these  no  doubt  produce 
marginal  gum  irritation,  a  fact  proven  by  the  relief  of  such  a  con- 
dition by  the  mere  continued  cleansing  of  the  teeth — i.  e.,  the  removal 
of  the  plaques. 

Talbot^  has  demonstrated  that  a  deep  pocket  may  normally  exist 
at  the  gum  margin  favoring  the  retention  of  food  and  other  debris. 

Mechanical  causes  produce  direct  irritation:  these  are  deposits  of 
salivary  calculus  resting  upon  the  gum  or  beneath  the  gum  margin; 
fillings  projecting  beyond  cavity  margin ;  gum  overlying  cavity  margins ; 
bruising  of  the  gum  margin  by  food  crowded  between  teeth  and 
removed  by  toothpicks;  the  fermentation  of  such  crowded  food;  the 
mechanical  action  of  toothpicks  or  floss  silk  improperly  crowded 
upon  the  gum  margin;  projecting  edges  of  artificial  crowns  or  bits 
of  cement  used  in  their  cementation;  toothbrush  bristles;  fragments 
of  toothpicks  or  oyster-shells,  etc. ;  rings  of  rubber  or  of  torn  rubber- 
dam  or  ligatures  left  in  position;  improper  contact  of  the  edges  of 
prosthetic  plates  or  appliances  about  the  necks  of  teeth;  injuries 
inflicted  by  rubber-dam  clamps,  wedges,  ligatures,  etc. 

The  action  of  any  of  these  causes  may  be  complicated  through  the 
infection  of  the  mechanically  irritated  part  by  oral  bacteria.  An 
excellent  example  occurred  in  the  editor's  practice.  A  perfect  gum 
margin  was  irritated  by  the  margins  of  a  gutta-percha  cap  used  as  a 

>  Dental  Cosmos,  1894.  2  jbid.,  1902.  s  Interstitial  gingivitis. 


MARGINAL  GINGIVITIS.  525 

remedy  for  hypersemia  of  the  pulp.  Pyogenic  organisms  produced  a 
marginal  suppuration  which  subsided  upon  removal  of  the  cap. 

Excessive  smoking  and  the  use  of  alcoholic  liquors  produce  local 
irritative  effects,  resulting  in  catarrhal  stomatitis  and  gingivitis. 

Lack  of  exercise  or  brushing  of  the  gums  produces  an  atonic  con- 
dition of  the  gum  margin,  predisposing  to  gingivitis  of  infective  char- 
acter. Too  persistent  brushing  with  stiff  brushes  may  be  equally 
injurious  by  causing  marginal  irritation. 

General  Causes.  It  is  quite  certain  that  in  conditions  of  general 
faulty  metabolism  substances  are  generated  in  the  system  or  are 
retained  by  reason  of  faulty  elimination,  and  which,  floating  about 
in  the  blood  stream,  act  as  irritants  to  the  pericementi  and  gum 
margins  about  the  teeth. 

Moreover,  the  pericemental  glands  seem  to  be  eliminating  organs 
which  may  become  overstimulated  and  thus  diseased. 

In  all  general  nutritional  disorders  parts  peripheral  to  the  circulation 
are  most  affected,  become  debilitated,  and  tend  to  a  degenerative 
metamorphosis  of  cells. 

Rhein  found  after  repeated  examinations  of  hospital  patients  that 
"marginal  gingivitis  was  an  accompaniment  of  typhoid  fever,  tuber- 
culosis, malarial  disorders,  acute  rheumatism,  pleurisy,  pericarditis, 
and  syphilis,  among  the  acute  diseases.  Of  chronic  nutritional  diseases, 
it  was  commonly  observed  in  cases  of  gout,  diabetes,  chronic  rheuma- 
tism, several  forms  of  nephritis,  scurvy,  chlorosis,  anaemia,  leukaemia, 
and  pregnancy.  Also  in  disorders  of  the  central  nervous  system  and 
following  the  administration  of  mercury,  lead,  and  iodine." 

Rhein  states  that  the  gingivitis  produced  by  any  of  these  diseases 
has  distinctive  features  which  may  even  serve  as  diagnostic  signs  os 
the  nature  of  the  general  malady. 

Talbot's  experiments  in  the  mercurialization  of  dogs  (see  Interstitial 
Gingivitis)  demonstrates  that  efforts  upon  the  part  of  the  perice- 
mentum to  eliminate  the  bichloride  of  mercury  result  in  a  non-septic 
pericementitis,  exhibiting  in  its  morbid  anatomy  the  characteristic 
round-celled  infiltration  of  inflammation. 

Black^  has  shown  that  a  gingivitis  produced  by  the  systemic  admin- 
istration of  potassium  iodide  may  be  proven  to  be  caused  by  its  elimi- 
nation by  the  pericemental  glands  by  test  of  the  gingival  secretion  for 
the  iodine  reaction. 

It  is  quite  reasonable  to  suppose  that  irritative  substances  originating 

1  American  System  of  Dentistry. 


52(5     PERICEMENTAL  DISEASES  BEGINNING  A  T  THE  GUM  MARGIN. 

in  the  body  and  floating  in  the  blood  stream  may  act  in  hke  manner. 
This  has  been  termed  autointoxication. 

Irritation  resulting  from  the  administration  of  mercury,  lead,  and 
iodine,  or  from  toxic  substances  absorbed  from  the  intestines,  is,  of 
course,  extrinsic  intoxication. 

It  has  been  claimed  by  Hunter,  Herschell,  Goadby,  W.  B.  Keyes, 
D.  D.  Smith,  and  others,  that  the  toxins  formed  by  oral  fermenta- 
tions and  the  septic  infection  of  the  stomach,  intestines,  etc.,  arising 
from  the  mouth  are  competent  to  excite  a  train  of  systemic  disturb- 
ances ending  in  a  general  malnutrition. 

Certain  accomplished  cures  of  such  states  by  constant  oral  prophy- 
laxis lend  plausibility  if  not  certain  proof  to  this  argument.  Still 
the  malnutrition,  whatever  its  cause,  oral  or  otherwise,  may  become 
a  predisposition  by  lessening  the  resistance  of  the  soft  parts  about 
the  teeth. 

While  it  is  evident  that  such  causes  are  competent  to  produce  a 
gingival  irritation,  it  is  probable  that  the  marginal  irritation  is  in 
large  measure  due  to  bacteria  present  in  the  mouth.  Probably  the 
mercurial  or  other  irritation  plays  the  part  of  a  predisponent. 

Loup^  has  shown  that  a  mercurial  stomatitis  involving  the  gum 
margins  may  be  relieved  by  the  use  of  washes  containing  mercuric 
chloride — i.  e.,  the  oral  exciting  cause — the  infection — is  removed  by 
the  use  of  a  germicide. 

A  variety  of  marginal  gingivitis  exists  under  the  name  of  stomatitis 
ulcerosa ;  the  cause  is  clearly  infective,  but  the  exact  bacterium  has  not 
yet  been  recognized.  It  tends  to  rapidly  penetrate  the  pericemental 
tissue.  The  gum  margin  has  a  pasty,  sloughing  appearance.  The 
ulceration  is  rapidly  cured  by  a  wash  consisting  of  mercuric  chloride 
in  hydrogen  dioxide  (1 :  2000). 

Pathology.  The  pathology  of  marginal  gingivitis  is  that  of  an 
inflammation  located  in  a  peculiar  situation — i.  e.,  in  the  marginal 
gum  tissue — and  tending  to  spread  into  the  deeper  interstitial  tissues. 
(See  Pathology  of  Interstitial  Gingivitis.) 

Symptoms.  The  symptoms  of  marginal  gingi\'itis  depend  upon  the 
cause,  ^^hen  mechanical  causes  are  acting  the  gum  presents  an 
inflamed  appearance;  it  is  swollen,  of  a  bright-red  or  purplish  color, 
very  sensitive  to  touch,  and  bleeds  readily. 

If  a  calculus  rest  against  the  gum  the  latter  may  present  a  raw, 
chronically  inflamed  surface  in  contact  wdth  it.     A  ragged,  red,  split 

1  Third  International  Dental  Congress,  Paris,  1900. 


MARGIXAL  GIXGIVITIS.  527 

margin  of  gum  is  often  associated  with  calculus  upon  the  labial  surfaces 
of  lower  incisors,  cuspids,  and  bicuspids,  and  upper  cuspids  and 
bicuspids.  At  times  the  lingual  surfaces  of  the  lower  incisors  present 
such  an  appearance.  If  subgingival  calculus  be  present  the  gum 
margin,  if  markedly  affected,  appears  loosened  and  is  of  a  flabby 
appearance  and  purplish  in  color.  In  some  cases  the  gum  margin 
appears  thickened  or  h^-pe^trophied. 

A  bloodshot  appearance — i.  e.,  enlargement  of  terminal  vessels — is 
often  seen  in  gingi\"itis. 

In  cases  due  to  unhygienic  conditions — i.  e.,  food  collections  or 
vitiated  secretions  about  the  necks  of  teeth — a  raw,  red,  outer  surface 
of  the  gum  margin  is  noted,  particularly  in  young  persons. 

In  stomatitis  ulcerosa  a  yellow,  pasty  ulceration  of  the  gum  margins 
may  occur.  It  is  rodent  in  character,  very  painful,  and  may  cause 
rapid  loss  of  the  pericementum  and  of  the  tooth.  In  gingivitis  due  to 
oral  infection  by  the  coccus  of  gonorrhoea  an  intense  gingival  inflam- 
mation with  looseness  of  the  teeth,  pyorrhoea  alveolaris,  and  profuse 
salivation  may  occur. ^ 

Rhein  describes  a  serpentine  line  of  inflammation  as  appearing  a 
short  distance  above  the  margins  of  the  gums  in  Bright's  disease  of 
the  kidneys.    He  considers  it  pathognomonic  of  this  disease. 

Prognosis.  If  the  case  has  run  an  acute  course  and  is  due  to  the 
action  of  mechanical  causes  plus  infection,  recovery  is  usually  prompt 
upon  the  removal  of  the  cause  and  sterilization  of  the  injured  part. 
In  the  chronic  cases  due  to  the  more  slowly  acting  mechanical  and 
infective  causes  combined^e.  g.,  salivary  calculus  plus  infection — 
much  interstitial  gingi^^tis  may  have  occurred  accompanied  by  peri- 
cemental and  alveolar  resorption.  This  constitutes  a  permanent  loss. 
If  the  gum  maroin  is  in  a  state  of  atonv  or  inflammation  as  the  result 
of  collections  of  bacteria,  etc.,  upon  the  cervices  of  the  teeth,  their 
condition  may  be  improved  by  frequent  cleansings  of  the  teeth. 

The  improvement  of  certain  chronic  malnutritional  disorders  may 
be  hoped  for  if  frequent  prophylaxis  be  practised  as  a  means  of  cause 
removal,  and  at  the  same  time  the  accumulated  waste  products  be 
eliminated  from  the  body  fluids  by  appropriate  means.  This  may, 
in  advanced  cases,  also  involve  the  treatment  of  diseased  organs. 

The  idea  of  systemic  infection  from  the  mouth  is  gaining  such 
headway  that  it  deserves  increased  prominence.  Even  should  its 
influence  be  overestimated  it  will  serve  as  a  strong  argument  in  present- 

1  Vines,  British  Journal  of  Dental  Sciences,  1903,  and  Dental  Cosmos,  1903. 


528     PERICEMENTAL  DISEASES  BEGINNING  A  T  THE  GUM  MARGIN. 

ing  tlie  subject  of  oral  prophylaxis  to  patients  who  unfortunately 
often  require  the  education  imparted  by  bitter  experience  in  order  to 
fully  grasp  its  importance. 

Treatment.  The  treatment  of  the  condition  consists  in  removing 
the  source  of  irritation  and  restoring  the  normal  circulation  in  the 
parts.  If  the  source  of  the  disorder  be  in  some  underlying  constitu- 
tional condition,  the  symptoms  may  be  ameliorated,  although  not 
entirely  cured,  by  the  correction  of  the  general  disorder. 

Cases  due  to  mechanical  irritation  are  commonly  confined  to  one  or 
several  teeth,  rarely  to  an  entire  denture,  except  cases  continued  in  con- 
sequence of  deposits  of  scaly  calculi  beneath  the  gum  margin.  Foreign 
bodies,  such  as  bristles  and  fragments  of  bone,  should  be  removed. 
Projecting  fillings  or  overhanging  crown  margins  should  be  made 
flush  with  the  general  tooth  surface.  Salivary  calculi  should  be 
removed. 

Antiseptic  mouth-washes  should  be  employed  frequently,  no  matter 
what  the  cause.  If  the  gum  tissue  be  soft  and  spongy,  showing  signs 
of  venous  hypersemia,  antiseptic,  astringent  mouth-washes  should  be 
freely  used: 

^ — Zinc,  chloric!.,  gr.  x. 

Aq.  nienth.  pip.,  Sj. — M. 

Increase  as  desired. 

The  above  preparation,  used  in  spray  from  an  atomizer  or  as  a 
wash  several  times  a  day,  is  an  excellent  local  application,  meeting 
both  indications.  Preparations  containing  carbolic  acid  and  allied 
substances  do  not  appear  to  act  happily  in  these  cases.  Prescrip- 
tions containing  eucalyptus  and  benzoic  acid  are  to  be  preferred : 


^ — Acid,  benzoic, 

3  parts. 

Tinet.  eucalypti, 

15     " 

01.  menth.  pip.. 

1      " 

Alcoliol, 

100     " 

Saccharin, 

2     "     -M. 

(Miller.) 

The  above  formula  diluted  one-half  is  agreeable  and  efficient. 
An  alkaline  1  per  cent,  salicylic  acid  wash  is  useful: 

9^ — Sodii  boratis,  5iss. 

Acidi  salicyliei,  gr.  xv. 

Aquae  menthse  pip.,  fSiij. — M. 

The  following  is  astringent  and  antiseptic: 

9; — Boroglycerini, 
Tinct.  kramerise, 
Tinct.  calendulse, 

Alcoholis,  eld    fSj.— M. 

Sig. — One  or  two  teaspoonfuls  to  a  small  glass  of  water. 


INTERSTITIAL  GINGIVITIS.  529 

Truman  advises  the  use  of  hydronaphthol  in  an  astringent  vehicle 
as  an  effective  germicide  for  use  by  a  patient: 


IJ: — Hydronaphthol, 

gr.  X. 

Glycerol, 

fSj. 

Alcohol, 

f3j. 

Aquae  destil., 

fgij.— M. 

Sig. — Use  as  wash  several  times 

a  day. 

(Peirce.) 

The  following  is  a  5  per  cent,  formaldehyde  solution  which  can  be 
used  as  a  mouth-wash,  having  astringent  and  antiseptic  qualities.  It 
is  also  useful  in  various  strengths  as  a  germicide  for  root-canals  and 
instruments.  A  formula  for  quantity  is  given,  which  may  be  reduced 
in  prescriptions: 

5fc- 


No.  1. 
-Thymol, 
Menthol, 

Siss. 

5ss. 

Oil  of  eucalyptus, 
Oil  of  gaultheria. 
Oil  of  cassia. 

Oil  of  cloves, 

dd 

fSiss. 

Alcohol, 

fsij.— M. 

No.  2. 

Formaldehyde,  40%  sol.. 
Boric  acid. 

Oj. 

Sodium  borate, 
Water, 

da 

Siij. 
Oij.— M. 

No.  3. 
Water  to 

gal.  j. 

Make  up  No.  1  first,  and  shake  well.  Place  No.  2  in  a  gallon  demi- 
john, and  shake  well;  add  No.  1  and  shake  again;  add  No.  3  and  shake 
well.  For  dispensing  this  may  be  filtered;  for  ordinary  use  this  is 
not  necessary.  For  mouth  use  a  teaspoonful  is  to  be  diluted  in  two 
ounces  of  water,  making  a  1 :  300  formaldehyde  solution. 

Equal  parts  of  listerine  and  ordinary  distillate  of  hamamelis  is  a 
useful  combination.  Glycothymolin  is  a  very  popular  proprietary 
mouth-wash.  All  mouth-washes  require  an  application  of  about  two 
minutes'  duration  at  least  twice  a  day  after  cleansing  the  teeth  in 
order  to  produce  the  best  effects.  As  this  is  somewhat  fatiguing  to 
the  oral  muscles  several  applications  may  be  made,  one  after  the  other, 
until  the  total  is  attained. 

INTERSTITIAL  GINGIVITIS. 

Definition.  Interstitial  gingivitis  may  be  defined  as  an  inflammation 
characterized  by  the  presence  in  the  connective-tissue  elements  of  the 
pericementum  and  gum  tissue  of  an  excessive  number  of  leukocytes, 
attracted  thither  by  a  general  or  local  irritation  of  the  tissues  men- 
tioned. 

34 


530    PERICEMENTAL  DISEASES  BEGINNING  A  T  THE  GUM  MARGIN. 


Causes.  The  causes  are  those  competent  to  produce  marginal 
gingivitis,  but  their  irritant  action  has  passed  beyond  the  gum  margin 
into  the  deeper  pericemental  tissue,  gum  tissue,  and  alveolar  process. 

The  causes  seem  to  be  divisible  into  local  exciting  (mechanical  and 
infective)  and  systemic  predisposing  (drug  action  and  autointoxication). 

Pathology  and  Morbid  Anatomy.  The  phenomena  of  inflammation 
are  produced.  The  bloodvessels  become  overfull,  diapedesis  of  leuko- 
c}i;es  into  the  interstitial  submucous  gum  tissue  occurs,  and  the  spaces 
are  filled  with  inflammatory  exudate.  The  papillae  become  enlarged 
and  the  epithelial  layer  undergoes  an  increase  in  formation  of  cells 
(hyperplasia).  The  gum  in  consequence  of  these  changes  becomes 
swollen,  its  color  deepened,  and  it  bleeds  readily. 

If  the  process  be  advanced  the  infiltration  extends  through  the 
alveolar  process  to  the  periosteum  and  gum  tissue. 


Fig.  465. 


Fig.  466. 


Fig.  467. 


Resorjitions  of  alveolar  process  due  to  interstitial  gingivitis,  caused  by  marginal  irritation 
from  excessive  filling  material.     (Radiographs  by  Price.) 

After  a  time  the  effects  of  continued  low-grade  inflammation  are 
expressed  in  resorption  of  bone  or  cementum,  or  both,  or  hypertrophy 
of  bone  or  cementum,  or  both,  or  the  two  processes  may  be  in  evidence 
at  the  same  time. 

If  at  any  time  pyogenic  infection  occur  at  the  gum  margin,  the 
purulent  phenomenon  of  pyorrhoea  alveolaris  is  produced. 

Following  resorption  of  the  alveolar  process  the  teeth  loosen,  more 
irritation  occurs,  infection  has  a  deeper  action,  calculi  may  form  on 
the  roots,  and  the  teeth  are  finally  lost. 

Talbot  describes  several  forms  of  bone  resorption  occurring  in 
interstitial  gingivitis: 

(a)  Lacunar  resorption  carried  on  by  the  osteoclasts  normally  lying 
upon  the  surface  of  the  bone.  Under  irritation  they  increase  in  number 
and  excavate  irregular  bays  in  the  bone  (Howship's  lacuna;).  These 
are  then  deepened  and  widened,  destroying  areas  of  bone.  (See 
Fig.  65.) 


INTERSTITIAL  GINGIVITIS.  531 

(6)  Perforating  canal  resorption  beginning  in  the  small  canals 
normally  perforating  the  trabeculse  of  bone  in  various  directions  and 
transmitting  the  bloodvessels  from  one  medullary  space  or  Haversian 
canal  to  another  (Volkmann's  canals) .  The  osteoclasts  widen  these, 
necessarily  reducing  the  substance  of  the  trabeculse  (Fig.  63). 

(c)  Hahsteresis  ossium,  beginning  with  a  decalcification  of  masses  of 
the  bone,  the  organic  matrix  being  for  a  time  undisturbed,  but  is  later 
removed.  This  is  a  local  expression  of  what  may  occur  in  other  bones 
of  the  body  in  the  condition  known  as  osteomalacia  (Fig.  66). 

Fig.  468.  Fig.  469. 


Fig.  468. — Longitudinal  section  of  gingival  border,  showing  round-cell  inflammation,  due  to 
mercury,  and  extending  to  the  inner  coat  of  the  bloodvessel,  and  also  plasma  mast-cells.  From 
a  dog.     (Talbot.) 

Fig.  469. — Endarteritis  obliterans:  A,  adventitia;  E,  elastic  tissue  between  middle  coat  and 
intima;  M,  muscular  coat ;  J,  thickened  intima.     (Talbot,  after  Kaufmann.) 

According  to  Talbot  premature  resorption  of  the  alveolar  margins, 
either  local  or  general,  is  due  to  this  process,  called  by  him  alveolar 
osteomalacia,  and  occurs  in  pregnancy  or  senility,  as  a  rule. 

He  states  that  the  decalcified  bones  may  be  recalcified  after  confine- 
ment in  pregnancy,  but  is  never  restored  in  senility. 

A  lesser  degree  of  irritation  may  set  the  osteoblasts  at  work  and 
cause  the  building  up  of  the  alveolar  process,  either  as  a  restoration  of 
resorbed  bone  or  as  an  hypertrophy  of  either  the  alveolar  process  or 
the  cementum  of  the  root  (hypercementosis). 

Endarteritis  obliterans  is  a  thickening  of  the  intima  of  an  artery 
or  capillary,  due  to  chronic  irritation  and  causing  a  lessening  of  the 
lumen  of  the  vessel,  even  to  the  point  of  obliteration  of  the  capillaries. 


532    P  ERIC  EM  EN  TA  L  DISEA  SES  BEGINNING  A  T  THE  G I  Wf  MA  RGIN. 

The  blood  flow  is  impeded  and  nutrition  of  cells  impaired.  Any 
cause  of  interstitial  gingivitis  may  produce  it:  in  all  cases  of  chronic 
interstitial  gingivitis  the  bloodvessels  are  so  diseased^  (Fig.  469). 

Treatment.  The  treatment  of  interstitial  gingivitis  is  either  that  of 
marginal  gingivitis  or  pyorrhoea  alveolaris.  The  description  is  intro- 
duced as  an  explanation  of  the  deep  action  of  causes  producing 
marginal  gingivitis,  and  of  the  manner  in  which  marginal  gingivitis 
leads  to  pyorrhoea  alveolaris  or  other  forms  of  pericemental  and 
alveolar  loss. 


Fig.  470. 


MARGINAL  ATROPHY  OF  THE  GUMS. 

In  advanced  age  there  exists  often  a  tendency  of  the  gums  to  shrink 
evenly  away  from  the  enamel,  exposing  the  cenientum.  Hopewell- 
Smith  describes  this  as  accom- 
panied by  fibroid  degeneration  of 
the  pericementum,  and  regards 
the  latter  as  a  purely  senile 
change. 

It  may  be  noted  upon  the  buc- 
cal side  only  of  a  denture  and  be 
due  to  vigorous  brushing. 

It  is  also  seen  localized  at 
cervices  next  to  a  space  from 
which  a  tooth  has  been  extracted. 
In  one  case  the  editor  saw  a 
slightly  hypertrophied  gum  dis- 
tinctly overlapping  a  cavity  mar- 
gin drawn  back  one-eighth  inch 
within  a  month  as  the  result  of 
extraction  of  the  adjoining  root. 

Apart  from  senile  changes  and 
possibly  even  including  them  these 
effects  seem  to  be  the  result  of  an  overstimulation  of  the  gums  resulting 
in  atrophy.  It  may  be  that  collections  upon  the  teeth  are  in  some 
degree  responsible.  The  gums  have,  for  the  most  part,  a  healthy  look^ 
but  are  in  a  condition  predisposed  to  pyorrhoea  alveolaris. 

There  seems  to  be  no  treatment  possible  beyond  careful  removal  of 
deposits  of  all  kinds  and  the  avoidance  of  excessive  brushing  of  the 


Recession  of  gum  in  senility;  beginning  decal- 
cification of  cementum;  alveolar  resorption  after 
extraction.  (Philadelphia  Dental  College  Mu- 
seum.) 


gums. 


1  Talbot. 


CHAPTER    XXIV. 

SALIVARY  AND  SERUMAL  CALCULUS. 

Calculi  are  more  or  less  hard  concretions  found  in  varjdng  situa- 
tions and  composed  of  inorganic  and  organic  matter  combined  in  an 
unknown  manner. 

As  related  to  the  teeth,  calculi  arise  from  the  following  recognized 
sources : 

1.  Obviously  from  the  saliva,  and  deposited  in  situations  which 
clearly  indicate  its  source  (salivary  or  ptyalogenic  calculus). 

2.  From  the  serum  of  the  blood  deposited  at  some  point  along  the 
side  of  the  root  between  the  gum  margin  and  the  apex  of  the  root,  and 
called  serumal  calculus.     Of  this  there  are  several  varieties: 

(a)  That  associated  with  a  probable  fermentation  and  an  altered 
secretion  from  the  gum  margin,  and  known  as  subgingival  calculus. 

(6)  That  occurring  in  situations  in  which  a  chronic  pus  flow  is 
found,  whether  apical  or  subgingival,  and  which  may  be  called 
pyogenic  calculus. 

(c)  That  found  upon  the  roots  of  teeth  at  a  point  to  which  saliva 
has  no  access  and  over  which  pus  does  not  flow,  and  which  is  therefore 
deposited  by  the  lymph  derived  from  the  blood,  and  to  which  the 
appellation  haematogenic  calculus  (Peirce)  is  applicable. 

These  several  names  will  be  adhered  to  in  further  descriptions  as 
having  definite  significance. 

SALIVARY  CALCULUS. 

Definition.  Salivary  or  ptyalogenic  calculi  are  hard  formations 
composed  of  calcium  salts  of  the  saliva  which  have  been  deposited  or 
precipitated  and  combined  in  an  unknown  manner  with  organic 
substances,  probably  mucin  or  globulin. 

Occurrence.  They  are  found  upon  the  surfaces  of  the  teeth, 
notably  in  situations  opposite  the  mouths  of  the  salivary  glands,  in 
the  ducts  of  the  muciparous  salivary  glands  (sublingual  and  sub- 
maxillary), and  upon  artificial  dentures.     A  photograph  of  a  plate^ 

1  Possession  of  Academy  of  Stomatology  of  Philadelphia. 


534  SALIVARY  AND  SERUMAL  CALCULUS. 

containing  an  enormous  mass  of  calculus,  the  result  of  seven  years' 
accumulation,  is  shown  in  Fig.  471. 

Varieties.  Clinically  two  distinct  varieties  of  salivary  calculus  are 
recognizable:  (1)  the  soft,  friable,  whitish-yellow  deposits  found 
chiefly  upon  the  buccal  surfaces  of  the  upper  molars  and  upon  the 
lingual  surfaces  of  the  lower  anterior  teeth;  (2)  dark-colored  and  hard 
deposits  found  more  frequently  in  the  latter  situation,  less  frequently 
in  the  former. 

Origin  of  Salivary  Calculus.  The  origin  of  salivary  calculus  may  be 
studied  from  several   standpoints:     (1)  the  formation  of    calculi  in 

other  parts   of  the  body;    (2)   an 
^  analysis  of  saliva  and  salivary  cal- 

culi; (3)  extra-oral  experiments 
upon  saliva  with  a  view  to  the  for- 
mation of  salivary  calculus  extra- 
orally;  (4)  the  changes  observed 
clinically  in  salivary  calculus  dur- 
ing its  deposition. 

Ziegler^  states  that  all  free  con- 
cretions  have  an  organic  basis  or 
nucleus    (inspissated    feces,    vege- 

Salivary  calculus  attached  to  a  lower  par-  ^       _^  .  .    ,  , 

tial  plate  worn  seven  years  without  removal.  table      material,      epithelial      SCalcS, 
Shows  form  of  sublingual  space.     Practice  of  ,      s 

Dr.  Ford,  Toulouse,  France.      (Specimen  in  mUCUS,    CtC.;. 
possession  of  Philadelphia  Academy  of  Stoma-  ^g    ^o    cholestcrin    gallstonCS    hc 

states  that  if  the  cholesterin  be 
dissolved  out  by  ether  a  yellowish,  organic  matrix  remains,  which 
retains  the  form  of  the  stone  and  presents  upon  examination  radiating 
spaces  formerly  occupied  by  the  crystals.  He  describes  the  formation 
of  the  gallstone  as  an  infiltration  or  incrustation  of  degenerated  organic 
matter  (epithehal  scales,  etc.)  with  cholesterin,  bile-pigment,  etc.,  to 
which,  after  a  nucleus  is  formed,  other  portions  are  added  in  like 
manner. 

Of  urinary  calculi  he  states  that  Ebstein  has  shown  an  organic 
substance  albuminous  in  nature  to  be  left  after  dissolving  out  the 
various  salts. 

In  stratified  calculi  this  stroma  also  shows  stratification.  Such  a 
stroma  may  be  seen  after  decalcification  of  a  bit  of  salivary  calculus. 

Analysis  of  salivary  calculus  shows  it  to  be  composed  of  about  22  per 
cent,  of  water  and  organic  matter  as  the  portion  removable  by  burning 

1  General  Pathology. 


SALIVARY  CALCULUS.  535 

the  calculus,  and  about  78  per  cent,  inorganic  matter  as  the  portion 
removable  by  decalcification  with  acids. 

Following  are  the  analyses  of  salivary  calculus  by  Stevenson  and 
Schehevetskey,  respectively:^ 

Soft  tartar  Hard  tartar  on 

on  molars.  .  lower  incisors. 

Water  and  organic  matter      ....       21.48  17.51 

Magnesium  phosphate    .....          1.31  1.31 
Calcium,  phosphate  with  a  little  carbonate 

and  trace  of  fluoride 77.21  81.18 

100.00  100.00 

Water  and  organic  matter       ....  22.07 

Magnesium  phosphate 1.07 

Calcium  phosphate 67.18 

Calcium  carbonate 8.13 

Calcium  fluoride 1.55 

100.00 

These  observers  are  practically  agreed  upon  the  substances  present 
in  calculus  as  mainly  calcium  phosphate  with  some  calcium  carbonate, 
calcium  fluoride,  and  magnesium  phosphate  combined  with  organic 
matter. 

Talbot  furnishes  the  following  analysis  of  serumal  calculus  by  J.  H. 
Salisbury:^ 

Water  and  organic  matter 32.24 

Magnesium  phosphate 0.98 

Calcium  phosphate 63.08 

Calcium  carbonate 3.70 

100.00 

According  to  Mitscherlich,^  parotid  saliva  contains  globulin,  but  no 
mucin,  and  contains  calcium  carbonate;  calcium  phosphate  being 
present  in  but  minute  amount.  The  submaxillary  saliva  contains  a 
large  amount  of  mucin,  which  gives  to  mixed  saliva  its  viscid  nature. 

Analyses  of  submaxillary  saliva  and  mixed  saliva  by  Bidder  and 
Schmidt  gave  the  following  results: 

Submaxillary  Saliva. 

Water 991.45 

Organic  matter 2.89 

Calcium  chloride  1  .  -„ 


Inorganic  matter 


Sodium  chloride 
Calcium  carbonate 


Calcium  carbonate         "| 

Calcium  phosphate         V ■'••^" 

Magnesium  phosphate   •'  

1000.00 


1  Talbot,  Interstitial  Gingi\atis.  "  Ibid. 

3  Halliburton,  Physiological  and  Pathological  Chemistry. 


536  SALIVARY  AXD  SERUMAL  CALCULUS. 


Mixed  Saliva. 

Water 995.16 

f    Epithelium 1.62 

organic  matter      {    soluble  organic  matter 1.34 

Potassium  sulphoeyanide 0.06 

Inorganic  matter  ]    Sodium,  calcium,  and  magnesium  phosphate .  0.98 


Sodium  and  potassium  chloride        .       .       .       0.84 

1000.00 

That  an  error  of  experiment  or  estimation  exists  in  these  analyses 
is  shown  by  the  fact  that  calcium  carbonate  is  not  mentioned  as 
existing  in  mixed  saliva,  while  it  exists  in  submaxillary  saliva:  this  is 
a  physical  impossibility. 

It  is  presumptive,  however,  that  calcium  carbonate  has  not  been 
specially  estimated. 

The  blood  contains  about  0.8  per  cent,  of  inorganic  salts  including 
those  found  in  salivary  calculi,  and  a  certain  percentage  of  them  is  also 
found  in  the  blood  corpuscles.  They  probably,  therefore,  exist  in 
body  cells  in  some  proportion. 

The  salts  are  also  taken  into  the  body  in  the  form  of  food.  Their 
appearance  in  the  various  excretions  and  secretions  of  the  body  is  to 
be  regarded  as  in  all  probability  an  effort  upon  the  part  of  the  system 
to  eliminate  a  superabundance  of  inorganic  material  from  the  body. 

The  ingestion  of  quantities  of  animal  or  vegetable  food  rich  in 
phosphates  or  the  excessive  liberation  of  the  phosphoric  acid  in  mal- 
nutrition may  produce  an  excessive  elimination  of  these  in  the  excre- 
tions and  cause  a  tendency  to  the  production  of  calculi  about  the  body. 
This  condition,  known  as  phosphaturia,  is  observed  in  certain  nervous 
diseases,  rachitis,  osteomalacia,  leukaemia,  gout,  and  rheumatism,^  in 
which  the  phosphaturia  is  s}Tnptomatic  of  an  excessive  catabolism; 
also  in  intestinal  disturbance  resulting  in  imperfect  assimilation  of 
food. 

Whether  taken  in  as  food  or  liberated  during  metabolism  it  is 
probable,  as  pointed  out  by  Talbot,  that  if  one  excretory  organ  fail  to 
perform  its  office  in  full  degree  another  must  take  up  its  work.  For 
this  reason  in  any  bodily  condition  affecting  elimination,  a  super- 
abundance of  inorganic  salts  may  appear  in  the  blood  and  hence 
in  the  saliva,  and  probably  in  even  the  secretions  from  the  gingival 
margins. 

That  the  deposit  of  calculus  is  mainly  dependent  upon  the  super- 
abundance of  calcium  salts  in  the  saliva  is  evidenced  by  the  fact  that 

^  Thompson,  Practical  Medicine. 


SALIVARY  CALCULUS.  537 

in  young  children  but  little  calculus  is  deposited  upon  the  teeth, 
though  the  oral  fermentation  is  not  lacking. 

If  a  bit  of  calculus  be  dried  and  then  burned  at  a  red  heat,  the  organic 
matter  present  will  burn  out,  the  calculus  retaining  its  form.  If  a 
similar  bit  be  subjected  to  a  dilute  acid  (1  per  cent,  nitric),  the 
inorganic  matter  will  be  removed,  the  calculus  will  float  to  the  top 
of  the  liquid,  and,  after  a  time,  remain  as  a  light  stroma  of  nearly 
the  original  form  of  the  piece. 

If  a  bit  of  calculus  be  transversely  ground,  it  is  seen  under  a  low- 
power  lens  to  present  a  laminated  appearance — i.  e.,  it  has  been 
deposited  in  layers  representing  periods  of  acti\'ity.  The  under 
surface  of  the  calculus  shows  a  concentric  formation.  Beneath  the 
mass  a  nidus  of  darker  calculus  may  be  found,  and  if  section  of  exten- 
sive calculi  be  made  the  greenish  deposits  may  be  seen  scattered 
through  the  mass.  Black  has  noted  the  presence  of  urates  in  nearly 
all  specimens  examined  by  the  murexid  test.  Foreign  bodies  are 
sometimes  entangled  in  the  mass.  Peirce  recorded  a  case  in  which 
a  small  clasp  plate  was  securely  fast- 
ened to  the  teeth,  and  the  patient 
denied  possession  of  such  a  sub- 
stitute. 

In  some  cases  extensive  salivary 
deposits  are  found  associated  with 
highly  offensive  odors — {.  e.,  putre- 
faction of  the  organic  matter  occurs 

as  a  part  of    the   process— indeed,  ~~  a,  nidus;  b,  calculus. 

bacteria    are   constantly  associated 

with  the  mass  and  may  furnish  their  quota  of  the  organic  matter. 
Extraneous  matters,  such  as  tobacco-smoke  or  other  pigments,  cause 
discoloration  of  the  mass.  With  data  relative  to  the  physical  and 
chemical  analysis  of  calculi,  the  mode  of  calculus  formation  may  be 
studied.  It  will  be  noted  that  the  necessary  elements  of  calculus 
formation  are  supplied  by  the  saliva  and  food  debris — i.  e.,  an  organic 
basis  is  furnished  in  which  calcium  salts  maybe  entangled, precipitated, 
or  chemically  combined. 

Mode  of  Calculus  Formation.  If  a  test-tube  be  filled  with  saliva  and 
allowed  to  remain  at  rest  for  several  days,  a  flocculent,  light-yellow 
precipitate  will  be  noted  at  the  bottom  of  the  tube.  If  the  supernatant 
fluid  be  drawn  off  with  a  pipette  and  the  precipitate  be  allowed  to 
dry,  it  will  be  found  possessed  of  the  chief  characteristics  of  calculus — 


538 


SALIVARY  AND  SERUMAL  CALCULUS. 


hardness,  friability,  a  light-yellow  color,  tenacity  of  adherence  to  objects 
with  which  it  is  in  contact,  and  capability  of  analysis  into  organic 
matter  and  inorganic  salts. 

Various  theories  are  held  as  to  the  mode  of  precipitation  of  the 
calculus  upon  the  teeth: 

1.  The  calcium  salts  are  held  in  suspension  by  carbon  dioxide.  As 
the  carbon  dioxide  escapes  the  calcium  salts  precipitate,  but  become 
combined  with  a  certain  percentage  of  the  albuminous  elements  of 
the  saliva — i.  e.,  globulin  and  mucin. 


Fig.  473. 


Fig.  474. 


Fig.  473.— Unclean  necks  of  teeth,  salivary  calculus,  and  green  stain.     (Philadelphia  Dental 
College  Museum.) 

Fig.  474.— a,  maxillary  sinus;  B,  duct  of  Steno;  C,  parotid  calculus;  E,  submaxillary  gland. 

2.  Burchard^  observed  that  lactic  acid,  as  well  as  acetic  acid  and 
mineral  acids,  has  the  property  of  coagulating  mucin.  If  to  a  test-tube 
half  filled  with  saliva  a  few  drops  or  more  of  a  1  per  cent,  solution  of 
lactic  acid  be  added,  a  cloudiness  will  appear  in  the  solution;  shred- 
like  coagula  of  mucin  are  formed,  which  slowly  agglomerate  and  rise 
to  the  surface  of  the  saliva.  If  the  amount  of  acid  be  increased,  the 
coagula  form  more  promptly.  If  the  coagulum  be  removed  and  dried 
it  is  found  upon  analysis  to  contain  calcium  salts. 


1  Dental  Cosmos,  1895. 


SALIVARY  GALCULUS. 


539 


The  combined  precipitation  of  calcium  salts,  owing  to  escape  of 
carbon  dioxide  and  the  coagulation  of  the  mucin  entangling  them,  is 
held  responsible  for  the  formation  of  the  calculi. 

3.  It  has  been  suggested  that  the  carbon  dioxide  in  the  air  expired 
from  the  lungs  causes  the  precipitation  of  the  calcium  in  the  saliva. 
That  this  is  an  error  is  seen  by  reference  to  analyses  of  calculi,  which 
would  be  largely  composed  of  calcium  carbonate  were  this  the  case; 
whereas  they  consist  largely  of  calcium  phosphate  pre-existent  in  the 
saliva;  moreover,  such  a  theory  fails  to  account  for  serumal  calculi. 

That  rest  or  relative  quiessence  of  the  saliva  is  necessary  for  the 
formation  of  calculus  is  shown  by  the  fact  that  it  occurs  at  points 
which  are  ordinarily  not  subjected  to  agitation — i.  e.,  buccal  surfaces 
of  upper  molars,  lingual  and  labial  surfaces  of  lower  incisors. 


C,  calculus;  S.  L.  C,  sublingual  cavity;  S.  L.  G.  L.,  sublingual  gland. 

Adhesive  precipitations  of  newly  formed  and  very  soft  calculus  form 
in  these  latter  situations  in  the  course  of  twenty-four  hours.  If  not 
removed  by  brushing  they  harden  and  thicken.  An  unused  side  of 
a  denture  often  accumulates  calculus  in  greater  degree  than  the  side 
used  for  mastication.  This  does  not  occur,  however,  if  the  brush  be 
used  properly  and  equally  vigorously  upon  both  sides. 

Burchard  has  pointed  out  that  irritations  of  various  natures  about 
the  teeth  and  gums  may  by  reflex  action  cause  secretions  of  fluid, 
abnormal  in  quantity  and  quality,  from  both  the  salivary  glands  and 
the  buccal  parietes  (glands  and  gum  margins). 

An  increase  of  oral  fermentation  is  commonly  associated  with  an 
excess  of  calculus  formation,  but  conditions  of  oral  fermentation  may 
be  seen  in  which  but  little  deposit  occurs.  The  mouths  of  many 
children  are  examples  of  this. 


540 


SALIVARY  AND  SERUMAL  CALCULUS. 


Kirk  has  pointed  out  that  there  may  occur  a  chemical  combination 
between  the  or^jjanic  and  inorganic  elements  of  the  calculus  somewhat 
analogous  to  that  occurring  between  calcium  salts,  etc.,  and  albuminoid 
materials  in  the  formation  of  calcoglobulin.     (See  p.  122.) 

Calculi  harden  with  age.  It  is  commonly  noted  that  soft  calculus 
may  be  readily  removed  with  a  brush.  Calculus  deposited  upon  lower 
teeth  within  a  week  or  two  after  a  thorough  cleansing  may  be  scraped 
away  as  a  cheesy  mass;  after  a  much  longer  time  it  comes  away  as  a 
hard  scale.  In  very  old  deposits  it  may  be  exceedingly  hard  and 
quite  firmly  attached  to  the  teeth. 

These  clinical  observations  lead  to  the  deduction  that  an  infiltration 
of  calcium  salts  occurs  in  the  dead  organic  stroma  of    the  calculus 


Fig.  476. 


Right  side,  abrasion  from  overuse;  left  side,  deposits  due  to  stagnation. 

analogous  to  that  occurring  in  dead  or  degenerative  tissue  throughout 
the  body  (calcareous  infiltration  or  degeneration).  Another  theory  is 
suggested — i.  e.,  that  a  firmer  chemical  combination  of  the  organic 
and  inorganic  elements  of  the  calculus  occurs  (following  the  theory 
suggested  by  Kirk),  density  being  thereby  increased. 

In  the  analyses  furnished  by  Stevenson  (p.  535)  it  will  be  seen 
that  hardness  is  in  part  at  least  due  to  an  increased  proportion  of 
inorganic  elements. 

Theoretically,  subgingival  calculi,  pyogenic  calcuH,  and  haemato- 
genic  calculi  formed  within  the  unbroken  pericementum  may  derive 
their  organic  material  from  the  secretions  or  necrotic  tissue  of  the  part, 
and  their  inorganic  material  (largely  phosphate  of  calcium,  carbonate 


SALIVARY  CALCULUS. 


541 


of  calcium,  and  sodium  biurate)  from  the  serum  of  the  blood  (serumal 
calculus).  In  the  case  of  simple  subgingival  calculus  the  saliva  may 
play  a  part  by  furnishing  the  necessary  calcium  salts  as  claimed  by 
Peirce,  but  this  does  not  seem  to  be  absolutely  proven,  nor  would  it 
seem  to  be  necessary;  indeed,  in  certain  cases  of  pyorrhoea  pockets 
located  about  lower  incisors  in  which  salivary  calculus  might  readily 
be  deposited,  and  from  which  both  salivary  and  serumal  calculus  has 
been  thoroughly  removed,  the  serumal  calculus  has  again  collected 
in  quantity,  while  the  salivary  calculus  has  not  been  redeposited. 

Pathological  Effects  of  Salivary  Calculus.  In  contact  with  the  mucous 
membrane  a  salivary  calculus  excites  first  marginal  gingivitis  and  later 
interstitial  gingivitis  and  its  effects.     (See  p.  530.)     There  is  some- 


FiG.  477. 


Fig.  478. 


Fig.  477. — Section  of  a  lower  incisor,  with  a  large  deposit  of  salivary  calculus  impinging  upon 
and  causing  inflammation  of  the  gum.     (Black.) 

Fig.  478.— Section  of  an  upper  molar,  with  deposit  of  calculus  on  its  buccal  surface,  causing 
inflammation  and  absorption  of  the  gum  and  lower  border  of  the  peridental  membrane  and 
alveolar  wall.     (Black.) 

times  in  this  stage  the  wavy,  gnawing,  uneasy  sensation,  associated 
with  mild  hypersemia,  and  the  pulp  being  reflexly  irritated  the  teeth 
respond  more  readily  to  thermal  stimuli.  The  gum  margin  is  inflamed, 
and  occasionally  pyogenic  organisms  cause  pus  formation.  The  gum 
margin  recedes  and  coincidently  a  resorption  of  the  alveolar  process 
is  produced.  More  calculus  is  deposited  and  the  process  proceeds 
until  much  of  the  alveolar  support  is  lost.  Micro-organisms  no  doubt 
aid  in  the  process. 

The  tooth  is  thus  progressively  loosened,  moves  about,  and  a  resultant 
interstitial  inflammation  of  the  remaining  pericementum  occurs;  as  a 
result  the  membrane  is  thickened  and  the  alveolar  process  partially 


542 


SALIVARY  AND  SERUMAL  CALCULUS. 


resorbed  (Fig.  480).  Increased  looseness  occurs  until  the  tooth  drops 
out  unless  mechanically  held  in  place.  As  soon  as  the  alveolar  loss  is 
considerable  infection  usually  occurs  and  suppuration  may  be  grafted 
upon  the  results  of  mechanical  irritation. 

The  entire  process  may  occupy  but  a  year  or  two;  in  other  cases 
the  atrophy  of  the  alveolar  walls  is  very  slow. 

Prognosis.  The  prognosis  of  this  condition  depends  upon  the  extent 
of  alveolar  atrophy.  If  the  loss  of  support  be  not  so  extensive  as  to 
cause  marked  loosening  of  the  tooth  or  teeth,  the  teeth  may  be  retained 
for  an  indefinite  period,  if  they  be  so  attached  to  neighboring  teeth  as  to 
render  them  firm.    If  left  unsupported  the  pericementum  is  certain  to 


Fig.  479. 


Fig.  480. 


Tf%^,;;li^'\ 


Fig.  479.— Sectional  illustration  of  a  heavy  deposit  of  salivary  calculus  on  a  lower  incisor,  with 
partial  destruction  of  the  alveolus  of  the  tooth.     (Black.) 

Fig.  480. — Sectional  illustration  of  lower  incisor  with  deposit  of  salivary  calculus  less  heavy 
than  that  shown  in  Fig.  477,  but  with  greater  destruction  of  the  alveolus.     (Black.) 


degenerate,  owing  to  the  increased  mobility.  The  alveolar  atrophy  will 
continue,  and  probably  infection  of  the  degenerated  pericementum 
occur.  Redeposit  is  almost  certain  unless  all  morbid  conditions  are 
removed  and  extraordinary  precautions  be  taken  as  regards  clean- 
liness. 

Treatment.  The  treatment  may  be  divided  under  three  heads: 
removal  of  deposits,  correction  of  the  effects  of  their  presence,  and  pre- 
vention of  their  recurrence.  The  sole  means  of  removing  salivary 
calculi  should  be  instrumental.  It  is  frequently  recommended  that 
mineral  or  some  of  the  organic  acids  be  used  to  soften  the  deposits  or 
facilitate  their  removal.  Anyone,  having  seen  a  case  in  which  a 
5  per  cent,  solution  of  sulphuric  acid  had  been  used  for  this  purpose, 
needs  no  further  warning  against  the  application.    Acid  solutions  will 


SALIVARY  CALCULUS. 


543 


certainly  soften  the  deposits,  but  at  the  same  time  inevitably  cause  a 
roughening  of  the  enamel  of  the  teeth  by  a  solution  of  the  calcium  salts. 


George  H.  Cushiiig's  scalers.  The  forms  and  general  character  of  these  scalers 
are  well  shown.  All  the  instruments  except  No.  6  are  intended  to  be  used  with 
the  push  stroke.  Nos.  1  and  2  are  specially  intended  for  application  to  the  pos- 
terior surfaces  of  lower  incisors;  they  are  also  admirably  adapted  for  removing 
calculous  deposits  below  the  gum  between  molars  and  bicuspids,  and  from  the 
posterior  surfaces  of  the  last  molars.  No.  2  can  be  passed  quite  to  the  extremity 
of  most  roots  with  less  disturbance  to  the  soft  tissues  than  a  thicker  or  more 
rigid  instrument  would  cause.  Nos.  3  and  4  are  for  removing  deposits  at  and 
below  the  gum  between  the  teeth,  particularly  the  lower  front  teeth.  They  can 
also  be  easily  used  upon  the  sides  of  the  roots  of  many  teeth,  being  passed  toward 
the  apex  of  the  root  in  a  line  nearly  or  quite  parallel  with  that  of  the  axes.  No.  5 
is  intended  to  be  passed  between  the  lower  front  teeth  at  or  near  the  gum  and 
then  directly  upward,  to  remove  the  deposits  on  the  proximal  surfaces.  No.  6  is 
a  hoe,  and  is  intended  to  be  passed  quite  to  the  apex  of  the  roots,  where  a  hoe 
is  desired. 

Fig.  482. 


Moose-hide  wheels. 


To  be  sure,  the  acid  does  affect  the  calculus  more  than  it  affects  the 
enamel,  but  the  roughened  surfaces  of  the  latter  not  only  invite  wide- 


544  SALIVARY  AND  SERUMAL  CALCULUS. 

spread  deposits  of  fermentable  material,  but  render  certain  the  more 
extensive  accumulations  of  calculi  in  the  future.  After  oral  sterilization 
the  gross  deposits  may  be  removed  by  means  of  large,  sickle-shaped 
scalers  and  curved  chisels,  nearly  all  used  with  a  draw  cut  (Fig.  482). 
The  instruments  should  have  sharp  edges  and  be  introduced  beneath 
the  deposits,  so  that  the  gum  be  not  unnecessarily  wounded.  The 
scaling  should  be  continued  until  every  surface  which  can  be  cleansed 
by  these  instruments  is  perfectly  smooth. 

For  the  proximal  surfaces  of  the  lower  anterior  teeth  the  fiat- 
bladed  instruments  (Fig.  481)  should  be  used  with  the  push  cut. 
Younger's  pyorrhoea  scalers  are  very  useful  (Fig.  494). 

For  the  removal  of  associated  subgingival  calculus  not  too  deeply 
placed  beneath  the  gum  a  No.  35  Darby-Perry  excavator  is  of  almost 
universal  utility.  It  is  used  with  the  draw  cut  for  the  most  part.  A 
pair  of  them  may  be  employed  and  made  safe-sided  by  rounding  one 
edge  if  desired  to  avoid  injury  of  the  gum  margin.  All  of  the  calculi 
visible,  and  all  that  can  be  detected  by  their  roughness,  are  thoroughly 
detached  and  scraped  away  by  these  instruments.  The  surfaces  of  the 
teeth  are  next  cleansed  with  pumice  made  into  a  paste  with  glycerin  to 
prevent  spattering.  The  paste  is  applied  to  the  surfaces  of  the  teeth 
with  rubber  cups,  or  Robinson's  brush  wheels  or  cups,  which  are  used 
to  cleanse  the  labial,  buccal,  and  such  lingual  faces  of  the  teeth  as  they 
will  reach  (Figs.  484  to  490).  The  lingual  surfaces  of  upper  and  lower 
incisors  are  cleansed  with  moose-hide  wheels  (Fig.  483)  and  wheel- 
brushes. 

The  approximal  surfaces  of  the  teeth  are  cleansed  with  fine  linen 
tape  or  floss  silk  charged  with  the  pumice  paste.  More  inaccessible 
parts  require  the  use  of  an  orange-wood  point  mounted  in  a  hand 
carrier.  It  is  advisable  to  repeat  the  polishing  with  precipitated  chalk 
and  the  same  carriers. 

After  cleansing,  the  associated  gingivitis  should  be  reduced  and  the 
parts  kept  sterilized  while  healing  by  means  of  an  antiseptic  astringent 
mouth- wash. 

The  prescriptions  given  on  page  528  answer  admirably. 

If  desired  the  operation  may  be  divided,  the  gross  deposits  and  sub- 
gingival calculus  being  removed  at  the  first  sitting.  After  a  few  days' 
use  of  the  mouth-wash  the  stains  and  bacterial  plaques  upon  the  teeth 
and  any  overlooked  deposits  may  be  removed.  Tincture  of  iodine 
painted  over  the  teeth  brings  the  deeper  stains  of  the  collections  into 
prominence. 


SALIVARY  CALCULUS. 


545 


Register  states  that  a  forcible  spray  of  1  per  cent,  hydrogen  dioxide 
used  after  the  appKcation  of  tincture  of  iodine  will  soften  the  stains 
and  render  them  more  readily  removable. 

The  smoother  the  surfaces  of  the  teeth  are  made,  the  longer  the 
redeposition  of  calculi  will  be  delayed. 

It  is  a  wise  measure  to  cleanse  the  teeth  before  any  long  series  of 
operations  is  undertaken,  and  as  a  prophylactic  measure  in  the  combat 
with  caries  and  pyorrhoea  alveolaris  the  operation  should  be  frequently 


Fig.  484. 


Fig.  485. 


Fig.  486. 


Fig.  487. 


Fig.  488. 


performed.  Indeed,  the  teeth  should  be  cleansed  with  pumice  fre- 
quently so  that  it  may  not  be  necessary  to  remove  actual  salivary 
calculus,  except  in  those  cases  in  which  it  collects  with  abnormal 
rapidity.     (See  prophylaxis  of  caries  and  of  pyorrhoea  alveolaris.) 

In  cases  of  very  rapid  recurrence  of  salivary  deposits,  evidence  of 
an  associated  systemic  condition  should  be  sought.  In  this  direction 
sialosemeiology  and  urinalysis  may  develop  data  worthy  of  attention. 
The  systemic  condition,  if  recognizable,  should  receive  appropriate 

treatment.     Free  water  drinking  is  advisable. 

35 


546 


SALIVARY  AXD  SERUMAL  CALCULUS. 


SUBGINGIVAL  CALCULUS. 

By  subgingival  calculus  is  meant  that  form  of  deposit  which  occurs 
beneath  the  free  gum  margin  and  between  it  and  the  tooth.  The 
deposits  consist  of  small  scales  or  granules,  usually  quite  smooth  and 
much  darker  (olive  green)  than  salivary  calculi  (Fig.  491). 

Composition.  They  consist  mainly  of  calcium  phosphate  combined 
witli  undetermined  organic  substances.     (See  p.  541.) 

Cause  and  Pathology.  It  is  probable  that  some  degree  of  marginal 
gum  irritation  first  occurs,  though  many  cases  of  an  apparently  healthy 
gum  with  a  scale  of  calculus  beneath  it  are  seen.  Whether  the  irritation 
arises  through  fermentations  about  the  unclean  necks  of  the  teeth  or 
as  the  result  of  an  effort  upon  the  part  of  the  gum  margin  to  eliminate 
waste  products  from  the  system  is  not  absolutely  certain. 


Fig.  491. 


■*  A"  :---^'  - '.'  V-'-'-;  ■■'11  >'  '1-  --^  -  ■ 


A,  subgingival  calculus;  B,  receding 
pericementum. 


Resorption  of  the  septum  of  bone  and 
recession  of  the  gum  between  the  central 
and  lateral  incisors,  caused  by  deposits 
of  serumal  calculus  under  the  gingivse. 
(Black.) 


The  theory  most  tenable  is  that  uncleanliness  exists;  fermentation 
of  the  mixed  marginal  collection  and  gum  secretion  occurs,  the  gum 
secretion  containing  calcium  salts;  these  are  precipitated  with  some 
organic  matter,  forming  a  calculus. 

Talbot  has  shown  that  a  natural  pocket  may  exist  at  some  aspect 
of  the  gingival  space  which  is  capable  of  harboring  collections  of 
foreign  material.  The  normal  gum  margin  closely  approximates  the 
tooth  and  has  an  apparent  protective  influence  over  the  portion  it 
covers.  For  some  reason,  such  as  a  lack  of  normal  friction  or  the 
presence  of  microbic  plaques  just  above  it,  the  gum"^may  lose  its 
normal  tone  and  the  calculus  deposition  be  favored.  Its  secretion  is 
also  probably  altered  in  quality. 


SUBGINGIVAL  CALCULUS. 


547 


Effects  and  Symptoms.  The  direct  effects  are  exerted  upon  the  gum 
margin.  The  mechanical  irritation  may  cause  the  gum  and  alveolar 
process  to  undergo  resorption,  the  calculus  being  exposed. 


Fig.  493. 


The  alveoli  irreparably  destroyed  by  calcic  inflammation.     (Black.) 

At  times  this  resorption  is  accompanied  by  evident  marginal  inflam- 
mation, at  others  the  gum  margin  has  a  normal  color,  but  the  resorbing 
portion  is  sharply  defined  by  a  fine  line  (or  crease)  from  the  normal 

Fig.  494. 


9  10  II     12  13  14  15 

Younger's  new  set  of  pyorrhcea  instruments.     (Revised  by  Dr.  Robert  Good.) 


gum  tissue.  In  a  more  advanced  stage  this  demarked  portion  appears 
sunken  or  atrophied  and  may  have  a  sort  of  semihyaline  redness 
characteristic  of  the  inflammation.    At  times  the  gum  margin  appears 


548  SALIVARY  AND  SERUM AL  CALCULUS. 

everted.  If  the  deposit  occur  on  only  one  side  of  a  root  the  gum 
resorption  may  be  confined  to  that  side. 

The  hngual  root  of  an  upper  molar  is  often  exposed  for  a  con- 
siderable portion  of  its  length  by  successive  deposits  of  calculi.  The 
same  is  true  in  other  situations,  notably  upon  the  labial  surface  of  a 
lower  incisor. 

If  the  deposit  be  generally  distributed  about  the  neck  of  the  tooth 
the  resorption  is  more  equalized. 

In  some  cases  the  bifurcation  of  roots  may  be  exposed  and  calculi 
deposit  in  that  situation. 

In  some  cases  the  gum  margin  becomes  simply  atonic  or  passively 
congested  and  is  pushed  away  from  the  teeth  by  large  masses  of  the 
calculus,  which  undergo  lateral  accretion.  It  appears  as  a  flabby, 
thickened,  loosened  gum  margin,  which  readily  draws  about  the  necks 
of  the  teeth  if  the  calculus  be  removed. 

Finally  pyogenic  infection  may  occur  about  the  calculus  and  the 
symptoms  of  pyorrhoea  alveolaris  be  implanted.  When  this  is  estab- 
lished, calculi  may  be  deposited  farther  up  the  side  of  the  root. 

Treatment.  The  calculus  should  be  removed  by  means  of  delicate 
scalers  used  with  either  the  push  or  draw  cut,  as  most  convenient, 
after  which  astringent  antiseptic  mouth-washes  should  be  prescribed. 
The  subsequent  frequency  of  removal  and  oral  prophylaxis  are  of 
great  importance. 

PYOGENIC  CALCULUS. 

Pyogenic  calculus  is  that  form  of  serumal  calculus  which  is  deposited 
at  parts  of  the  tooth  root  over  which  pus  more  or  less  continually 
flows. 

In  chronic  apical  abscess  the  root  end  may  become  encrusted  with 
it,  and  in  those  cases  in  which  apical  abscess  discharges  along  the 
pericemental  tract  it  is  common  to  find  over  the  area  fine  granular 
deposits  which  vary  in  color  from  a  light  yellow  to  a  reddish-brown. 

The  same  is  true  of  active  pyorrhoea  pockets. 

This  calculus  prevents  the  healthy  apposition  of  the  gum  tissue  to 
the  roots,  probably  because  of  its  irritant  and  infective  nature  (Figs. 
432  and  495). 

Treatment.  All  such  calculi  should  be  removed  by  whatever  means 
possible,  which  may  necessitate  scraping  the  root  end  or  its  side,  or 
even  the  amputation  of  the  apical  end  of  the  root.  In  some  cases 
aromatic  sulphuric  acid  may  dissolve  it.     (See  p.  487.) 


HEMATOGENIC  CALCULUS.  549 

HEMATOGENIC  CALCULUS   (Syn.  Sanguinary  Calculus). 

This  form  of  serumal  calculus  occurs  in  the  so-called  gouty  peri- 
cementitis, a  form  of  pericemental  abscess. 

It  may  occur  in  the  absence  of  apical  abscess  or  a  primary  pyorrhoea 
alveolaris,  and,  therefore,  at  points  not  acted  upon  by  saliva  or  pus; 
hence  it  must  be  deposited  by  the  blood  through  the  lymph. 

Miller^  has  offered  a  satisfactory  evidence  of  this  in  a  description 
of  a  case  of  impacted  cuspid  well  embedded  in  the  bone,  and  not  in 
any  way  exposed  to  either  saliva  or  pus  influence  except  that  at  a 
point  over  the  cusp;  the  gum  underwent  suppuration  for  a  short  time. 
The  crown  had  undergone  resorption  showing  local  irritation,  and  an 
olive-green  calculus  had  formed  upon  the  middle  third  of  the  root. 
Cases  of  pericemental  abscess  have  been  noted  opening  upon  the  gum 
face  and  presenting  dark-green  calculi  upon  the  root  in  that  situation. 
(See  gouty  pericementitis.) 

Peirce  found  in  such  deposits  a  proportion  of  sodium  urate  as  shown 
by  the  murexid  test  and  the  cases  associated  with  goutiness  of  the 
patient. 

While  such  deposits  may  not  cause  immediate  irritation  they  may 
in  time  excite  inflammation  and  necrosis  of  tissue  resulting  in  a  dis- 
charge of  glairy  material  representative  of  the  condition.  This  form 
of  dental  disease  will  be  further  discussed. 

1  Dental  Cosmos,  1901. 


CHAPTER   XXV. 
PYOERHCEA  ALVEOLAEIS. 

While  the  term  pyorrhoea  alveolaris  implies  but  one  symptom 
common  to  several  distinct  varieties  of  disease  of  the  pericementum, 
that  of  a  flow  of  pus  from  the  alveolus,  it  is  generally  understood  as 
a  term  descriptive  of  degenerative  conditions  which  have  some  distinc- 
tive features;  these  are  a  progressive  loosening  of  the  teeth  attended  by 
a  loss  of  the  retentive  structures,  alveolar  walls,  and  pericementum,  the 
loosening  of  the  teeth  being  in  a  majority  of  cases  attended  by  a  flow 
of  pus  from  the  margin  of  the  affected  alveolus,  and  by  deposits  of 
calculi  upon  the  sides  of  the  denuded  roots.  The  disease  ceases  spon- 
taneously with  the  loss  of  the  teeth;  the  resorption,  loss,  or  atrophy 
of  the  alveolar  wall  being  arrested  at  any  period  of  the  disease,  if  the 
affected  tooth  be  extracted. 

Causes.  The  several  clinical  varieties  of  this  disorder  all  seem  to 
be  associated  with  an  obvious  infection  which  in  turn  has  found  a 
favoring  condition  in  a  degenerative  state  of  the  pericementum  or 
gum  margin  of  one  or  more  teeth.  While  this  is  probably  true, 
investigations  in  this  direction  have  proven  negative  in  so  far  as  the 
determination  of  a  specific  bacterium  is  concerned. 

Galippe  and  jNIalassez,  Miller,  Black,  Goadby,  Younger,  Cook,  and 
others  have  all  failed  to  definitely  isolate  such  a  specific  bacterium. 
The  closest  approach  to  a  demonstration  yet  made  was  the  determi- 
nation by  Kirk  of  the  presence  of  a  pure  culture  of  the  diplococcus 
pneumoniae  in  a  few  cases  of  freshly  opened  pericemental  abscesses 
(which  see). 

The  investigations  of  Goadby,  however,  do  not  confirm  this  as  a 
cause  of  pyorrhoea  alveolaris  in  general,  but  rather  point  to  the  prob- 
ability that  the  cause  may  be  found  among  other  oral  bacteria,  possibly 
thread  forms  or  some  of  the  blastomycetes. 

Mr.  Sydney  Vines^  reports  a  case  of  intense  suppurative  stomatitis 
and  gingivitis  with  great  salivation  due  to  gonorrhoeal  infection  by  the 
medium  of  the  hands  and  a  toothpick  in  a  patient  suffering  from 
gonorrhoeal  urethritis.    The  gonococcus  was  found  in  the  mouth. 

1  British  Journal  of  Dental  Science,  1903. 


PYORRHCEA  ALVEOLARIS.  551. 

This,  of  course,  has  no  definite  relation  to  ordinary  pyorrhoea. 

Curtis^  believes  obstinate  cases  of  the  disease  to  be  either  caused 
by  or  aggravated  by  tertiary  syphilis.  He  bases  his  belief  upon  ob- 
servations of  fresh  blood  which,  he  states,  upon  the  authority  of  Dr. 
Robert  L.  Watkins  (New  York  City),  contains  syphilitic  spores. 

"  Egg-skin  "  eschar  is  the  oral  pathognomonic  sign. 

The  local  infection  in  nearly  all  cases  is  of  so  mixed  a  type  as  to  render 
it  at  present  uncertain  whether  the  liquefaction  of  the  peridental  mem- 
brane, etc.,  is  due  directly  to  the  pyogenic  organisms  present  in  the 
pus  formed  or  to  other  oral  bacteria  of  uncultivable  type  which  may 
irritate  the  process,  after  which  pyogenic  organisms  may  enter  and  form 
pus.  The  fact  that  pyorrhoea  alveolaris  is  seldom  found  fully  estab- 
lished before  thirty  years  of  age,  but  is  common  after  that  period,  and 
that  it  occasionally  occurs  in  youth  or  even  in  childhood  in  association 
with  some  pronounced  systemic  state  or  disease,  strongly  indicates  a 
systemic  factor  in  the  more  pronounced  forms  of  the  disease.  It  is 
probable  that  the  various  systemic  diseases — e.  g.,  rachitis  in  childhood, 
Bright's  disease,  anaemia,  or  neurasthenia  in  adults,  etc. — have  a  degen- 
erative influence  over  the  pericementum  in  one  of  two  ways:  1.  By 
introducing  the  factor  of  retention  of  normal  or  abnormal  waste 
metabolic  products  within  the  body  fluids  which,  presented  as  food 
to  the  pericemental  cells,  act  as  irritants  (autointoxication), 

2.  Through  a  possible  deprivation  of  the  pericemental  tissue  of 
necessary  nutritive  material  (tissue  starvation) — e.  g.,  as  in  anaemia. 

It  is  a  well-known  fact  that  peripheral  nutrition  is  disturbed  by 
systemic  conditions — e.  g.,  the  rapid  falling  out  of  quantities  of  the 
hair  during  periods  of  excessive  drain  upon  the  system,  as,  for  example, 
during  lactation. 

At  other  periods  no  such  result  may  be  noted.  The  presumption  is 
that  a  disturbed  peripheral  nutrition  or  circulation  from  any  cause 
renders  the  part^  affected  less  resistant  to  the  action  of  the  micro- 
organisms. 

The  investigations  of  Michaels  and  Kirk  upon  the  composition  of 
saliva  in  various  systemic  states  throws  much  light  upon  the  possibility 
of  the  presence  of  the  before-mentioned  irritants  in  the  blood  fluid. 
Kirk^  reports  the  finding  of  quantities  of  sodium  oxalate  in  the  urine 
of  certain  patients  suffering  from  malnutrition  and  neurasthenia. 
These  later  followed  by  the  appearance  in  the  saliva  and  urine  of 
calcium  oxalate.    These  are,  of  course,  derived  from  the  blood.    The 

1  Dental  Cosmos,  1901.  2  ibid.,  July,  1903. 


552  PYORRHCEA  ALVEOLARIS. 

presence  of  sodium  urates  in  the  blood  in  gout  is  well  established. 
Using  these  substances  then  as  a  foundation  for  argument,  it  is  seen 
that  no  reason  exists  why  these  (and  other  waste  products  as  well) 
should  not  float  through  the  capillaries  and  lymph  channels  or  even 
the  glands  of  the  pericementum,  and  produce  irritation  which  may  be 
followed  by  atrophic  or  hyperaemic  changes  in  that  tissue.  These 
changes  are  well  known  to  lead  to  degeneration,  and  degeneration 
lessens  resistance.  At  this  point  the  micro-organisms  produce  active 
efiFects  which  previously  are  resisted.  In  this  connection  the  fibroid 
degeneration  of  the  pericementum  due  to  age,  demonstrated  by  Hope- 
well-Smith, should  have  some  consideration  as  a  predisposing  cause 
at  the  proper  age. 

It  is  not  to  be  supposed  that  local  causes  are  not  competent  to  produce 
pericemental  degenerations — e.  g.,  such  causes  as  malocclusion,  over- 
use, abuse,  and  disuse  of  teeth ;  the  lack  of  friction  necessary  to  maintain 
the  normal  tone  of  the  gums;  the  excess  of  friction  in  some  cases. 

The  presence  of  fermentable  material  about  the  necks  of  the  teeth, 
particularly  those  of  the  narrow-necked  variety,  causing  the  precipita- 
tion of  calculus,  may  all  excite  the  degenerations  following  chronic 
irritation,  and  thus  favor  the  development  of  the  bacteria  producing 
pyorrhoea. 

It  has  been  argued,  notably  by  D.  D.  Smith,  that  if  the  teeth  be 
frequently  thoroughly  cleansed  of  all  deposits  of  all  sorts  the  pyorrhetic 
conditions  will  be  cured.  The  success  which  seems  to  attend  the  use 
of  the  rc-rays  and  high-frequency  electric  current  in  this  condition  is 
also  argument  that  the  cause  may  be  killed  out  by  local  treatment 
alone.  It  does  not  follow,  however,  that  a  cure  by  removal  of  a  cause 
implies  a  lack  of  predisposition  on  the  part  of  the  tissues  of  a  part  or 
individual.  The  tendency  in  some  cases  to  relapse  unless  the  cause 
be  continually  removed  is  a  proof  of  this  fact. 

It  has  been  shown,  on  the  other  hand,  that  intelligent  attention  to 
systemic  conditions  has  been  followed  by  amelioration  or  in  some  cases 
even  cure  of  the  pyorrhoea  when  local  treatment  alone  (apart  from 
constant  attention)  has  failed — i.  e.,  an  increased  resistance  of  the 
tissues  to  the  bacteria  present  has  been  brought  about  by  the  systemic 
treatment. 

The  argument  that  pyorrhoea  alveolaris  is  of  purely  local  origin, 
because  it  disappears  after  the  tooth  is  extracted,  is  no  more  sound 
than  would  be  the  argument  that  gout  in  the  great  toe  is  of  local  origin 
because  it  disappears  with  the  amputation  of  the  leg.     Pyorrhoea  is 


PYORRH(EA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     553 

a  disease  of  the  dento-alveolar  joint  (the  pericementum),  and  extrac- 
tion eHminates  that  joint. 

It  is  also  argued  that  the  local  infection  is  competent  to  produce 
not  only  the  gingivitis,  but  also  by  the  production  of  toxins,  either  in 
the  oral  cavity  or  at  some  point  in  the  alimentary  canal,  to  produce 
the  systemic  malnutrition. 

When  the  long  continuance  of  oral  infection  is  considered,  this  view 
is  entitled  to  great  respect,  but  the  general  predisposition  must  again 
be  a  factor  in  the  advance  of  the  disease. 

In  brief  it  may  be  stated  that  the  infectious  nature  of  pyorrhoea 
alveolaris  is  becoming  more  established,  albeit  not  yet  fully  scientific- 
ally proven,  and  that  the  causes  require  a  local  predisposition  for  their 
action.  This  local  predisposition  may  be  the  outcome  of  local  sources 
of  irritation  and  degeneration  alone  or  be  produced  by  waste  products 
floating  in  the  blood  stream,  etc. 

Clinically,  fully  established  cases  of  pyorrhoea  alveolaris  may  be 
divided  into  two  classes :  (1)  cases  associated  with  a  primary  gingivitis 
and  with  the  formation  of  hard,  scaly,  dark,  annular  calculi  beneath 
the  gum  margin  (subgingival  calculus),  the  pockets  not  usually  extend- 
ing far  beyond  the  deposits;  (2)  cases  beginning  with  a  marginal 
gingivitis  and  apparently  not  dependent  upon  the  association  with 
calculus,  though  frequently  complicated  by  it;  (3)  cases  having  an 
apparent  origin  at  some  point  between  the  gingival  margin  and  the 
apical  tissue,  the  gingival  margin  at  first  being  apparently  intact. 

It  is  probable  that  the  nature  of  the  infecting  agent  in  these  types 
are  different  or  that  in  the  event  that  they  may  be  proven  to  have  a 
similar  origin  the  tissues  react  differently  to  them,  either  partially 
resisting  them,  forming  calculus  as  a  result  of  the  irritation,  or  rapidly 
giving  way  to  them,  permitting  a  deep  action. 

In  the  absence  of  known  causes  the  conditions  may  be  divided 
according  to  their  clinical  expressions. 

In  the  consideration  a  pus  flow  due  to  apical  abscess,  lateral  abscess 
upon  a  perforation,  or  that  due  to  obvious  salivary  calculus  is  excluded. 
(For  these  see  under  proper  headings.) 

PYORRHCEA  ALVEOLARIS  BEGINNING  AS  A  MARGINAL  GINGI- 
VITIS AND  ASSOCIATED  WITH  SUBGINGIVAL  CALCULUS. 

Causes.  The  causes  of  this  condition  are  those  predisposing  and 
exciting  causes  of  marginal  gingivitis  which  have  been  described. 
(See  p.  524.)      Several   local   factors  have  to  be  considered   in  this 


554 


PYORRHCEA  ALVEOLA RIS. 


connection:  (1)  the  marginal  infection;  (2)  the  irritative  effects  of  any 
calcuhis  tliat  may  l)e  formed;  (3)  the  deep  infection  by  pyogenic 
organisms;  (4)  the  modification  of  the  progress  of  the  disease  by  the 
attendant  loosening  of  the  teeth  and  death  of  the  pulp. 

Clinical  History,  Pathology,  and  Symptoms.  There  is  usually  an 
unclean  condition  of  the  teeth  (Fig.  473);  infection  exists  either  in 
tenacious  films  of  bacteria  attached  to  the  necks  of  the  teeth  and 
requiring  reasonably  close  observation  for  their  detection,  or  in  masses 
of  detritus  readily  noticeable.  Subgingival  calculus  is  obviously 
present. 


Fig.  495. 


Serumal  calculus,  showing  stalactite-like  formations.     (Talbot.) 

The  gum  margin  may  be  atrophied  and  inflamed,  or  it  may  have 
a  fairly  normal  appearance.  When  the  gum  margin  is  pressed  upon, 
pus  may  be  squeezed  out  in  variable  quantity. 

It  is  assumed  that  the  local  infection  brings  about  fermentation  at 
a  point  beneath  the  gum  margin,  and  that  formation  of  su^bgingival 
calculus  occurs,  followed  by  pyogenic  infection  and  pus  formation. 

The  gum  may  now  be  resorbed  and  the  calculi  be  exposed.  In  this 
manner  the  bifurcations  of  the  roots  may  be  uncovered  and  calculi  be 
deposited  in  that  situation.  The  resorption  may  only  be  confined  to 
one  side  of  a  root  and  be  the  result  of  several  successive  depositions 
which  may  remain  when  the  gum  recedes,  or  which  may  be  removed 


PYORRHOEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     555 

and  again  be  deposited  (Fig.  493).  In  this  way  the  side  of  the  root 
may  be  exposed  nearly  to,  and  in  some  cases  quite  to,  the  apex.  In 
such  cases  the  pus  pockets  may  not  be  deep  and  the  pus  formed  may 
readily  be  washed  away.  Instead  of  this  the  pericementum  may  be 
progressively  destroyed  by  suppuration  and  the  gum  margin  remain 
practically  intact.  In  these  cases  the  pus  flow  is  more  abundant,  a 
deep  pocket  is  formed,  extending  a  third  or  even  two-thirds  or  more  of 
the  length  of  the  root.  It  is  common  to  find  beads  of  calculus  deposited 
along  the  side  of  the  root  and  presumably  of 
serumal  origin,     (See  pyogenic  calculus.) 

These  inflammatory  disturbances  necessarily 
involve  an  interstitial  gingivitis  or  infiltration  of 
leukocytes  into  the  interstitial  connective  tissue 
of  the  gum.  As  pointed  out  by  Talbot,  resorp- 
tion of  various  kinds  and  at  times  constructive 
changes  accompany  such  an  inflammation.  (See 
interstitial  gingivitis.)  These  results  are  noted 
in  connection  with  this  variety  of  pyorrhoea  alveo- 
laris.  In  the  early  stages  of  the  disease  the  probe  gai  root  of  molar  largely 
usually  fails  to  discover  uncovered  alveolar  bone,  '^^'^^'is'^-    Treated  by  am- 

''         _  _  putation.     (Price.) 

although  it  may  do  so.     If  not  uncovered  its  loss 
is  due  to  resorption ;  if,  however,  necrotic  and  bare  alveolar  bone  be 
found  it  is  undergoing  a  molecular  necrosis  under  the  influence  of  the 
pyogenic  organisms. 

In  some  cases  the  pericementum  may  be  destroyed  at  the  cervical 
third  of  the  root,  the  alveolar  process  may  be  resorbed  on  its  inner 
surface,  and  an  accompanying  constructive  irritation  may  cause  the 
deposition  of  bone  upon  the  outer  aspect  of  the  alveolar  process;  the 
gum  margin  is  also  thickened  by  cell  proliferation.  The  condition 
imparts  the  appearance  of  hypertrophy  of  the  gum  and  gum  margin 
(Fig.  497). 

When  about  one-half  or  more  of  the  root  has  been  stripped  of 
pericementum  and  deprived  of  alveolar  support,  looseness  and  extru- 
sion of  the  tooth  become  marked.  The  teeth  are  nearly  always  looser 
than  normal,  even  in  the  early  stages. 

The  advance  of  the  disease  now  becomes  more  rapid;  the  undue 
mobility  and  malocclusion  of  the  tooth  excite  an  inflammatory 
reaction  beyond  the  directly  infected  part,  so  that  soreness  and  loose- 
ness are  further  increased.  Extraction  at  the  later  stages  reveals 
a  thickened  apical  pericementum  as  the  sole  attachment  to  the  bone. 


556 


PYORRH(EA  ALVEOLARIS. 


Fig.  497. 


After  the  looseness  of  the  tooth  becomes  marked,  the  pulp  of  the  tooth 
undergoes  hyperjemic  changes,  reacts  to  thermal  stimuli,  and  is  often 
killed  by  strangulation  of  its  vascular  supply.    Pulp  nodules  often 

are  formed  before  its  death.  Infection  of 
the  dead  pulp  readily  occurs,  and  septic 
apical  pericementitis  arises.  The  symp- 
toms of  the  latter  condition  are  modified, 
according  to  the  facility  with  which  the 
pus  finds  vent  along  the  degenerating 
pericementum.  The  disease  proceeds 
until  the  affected  tooth  or  teeth  are  cast 
out,  the  alveolar  walls  and  pericementum 
having  entirely  atrophied.  The  disease 
ceases  with  the  loss  of  the  affected  teeth, 
leaving  a  flattened  or  absent  alveolar  ridge 

brane  and  eversion  of  the  alveolar  cOVCred  by  a  maSS  of  lliore  Or  IcSS  SpOUffy 
wall,   with  thickening  of  its  border:  .  r        Oi/ 

a,    serumal    calculus;     b,    thickened    gUm  tlSSUC. 

oavit^y.  °(Biack^  ^^°  ^^  ^^  '  '^'  ^"^       '^^^  duration  of  this  disease  may  be 

months  or  years,  and  a  number  of  teeth 
may  be  affected  at  once.  A  general  subcatarrhal  condition  of  the 
mouth  usually  attends  the  disease.  The  presence  of  pus  often  im- 
parts to  the  breath  a  peculiar,  sweetishly  fetid  odor  which  may, 
however,  be  masked  by  an  odor  of  putrefaction. 


Section  of  an  upper  incisor,  showing 
destruction  of    the  peridental  mem- 


FiG.  498. 


Fig.  499. 


Section  of  an  upper  molar  with  its  alveolus, 
•etc.,  showing  deposit  of  serumal  calculus 
under  the  gingival  borders:  a,  a,  serumal  cal- 
■culus.     (Black.) 


Section  of  an  upper  incisor,  showing  at  a,  a, 
a  deposit  of  serumal  calculus  within  the  free 
margin  of  the  gum.     (Black.) 


In  a  number  of  cases  of  deep  pyorrhoea  pockets  an  infection  of  the 
alveolar  structure,  or,  at  least,  of  the  tissue  remaining  over  the  deepest 
portion  of  the  pocket,  may  occur,  and  an  abscess  form  which  dis- 
charges by  a  fistula  through  the  labial  or  lingual  aspect  of  the  gum. 


PYORRHCEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     557 

It  is  to  be  regarded  as  an  abscess  secondary  to  a  primary  pyorrhoea 
alveolaris.  The  passage  of  a  silver  probe  through  the  two  sinuses  at 
once  will  reveal  this  (Fig.  500). 

In  one  case  of  pyorrhoea  alveolaris  of  the  variety  under  consideration 
the  pocket  existed  upon  the  mesobuccal  aspect  of  a  right  lower  third 
molar.  The  second  and  first  molars  were  absent.  The  pus  dissected 
away  the  periosteum  of  the  bone  and  formed  a  large  abscess  over  the 
entire  area  of  bone  between  the  third  molar  and  second  bicuspid. 
After  evacuation  of  the  abscess,  the  probe  was  passed  through  it  to 
the  pyorrhoea  pocket  (Fig.  501). 

While  dental  caries  may  occur  with  pyorrhoea  alveolaris,  it  is  usual 
to  find  the  teeth  of  the  most  highly  organized  structure.  The  pulp 
tissue  is  usually  increased  in  density,  and  there  is  a  tendency  to  the 
constructive  changes,  secondary  dentine,  nodules,  etc.,  and  the  inevi- 
table degenerative  changes  following  these  diseases. 


Fig.  500. 


Fig.  501. 


Gingival  abscess  secondary  to 
pyorrhoea  alveolaris.  C,  calculus  in 
pyorrhcEa pocket;  F,  fistula  leading 
to  pocket  PP;  B.boneon  lingual  side. 


Diagram  of  abscess  secondary  to  pyorrhoea  alveo- 
laris (see  text).  PP,  pyorrhoea  pocket;  AC,  cavity 
of  secondary  abscess;  B,  bone. 


It  has  been  contended  that  these  pulps  are  responsible  in  a  measure 
for  the  pyorrhetic  condition,  and  it  is  possible  that  they  may  by  reflex 
action  influence  the  tissue  nutrition  of  the  pericementum  and  gum 
margin,  though  the  contrary  process  is  quite  as  probable.  If  the  pulps 
be  degenerated  their  removal  aids  the  cure  of  the  disease  by  diverting 
the  blood  they  receive  into  the  pericemental  bloodvessels.  This  prob- 
ably counterbalances  the  effects  of  the  endarteritis  obliterans.  (See 
interstitial  gingivitis.) 

It  is  also  true  that  calculus  does  not  seem  to  form  as  readily  upon 
a  devitahzed  tooth  as  upon  one  containing  a  vital  pulp;  it  does  form 
at  times,  however. 

Diagnosis.  The  diagnosis  is  easily  made  when  the  disease  is  estab- 
lished by  observance  of  the  phenomena  just  described.    A  persistent 


558  PYORRHCEA  ALVEOLARIS. 

gingivitis  witli  an  exaggeration  of  the  space  between  the  tooth  and 
gum  margin  means,  as  a  rule,  a  future  pyorrhoea.  The  same  is  true 
of  a  receding  gum  margin  constantly  associated  with  an  uncleanly  tooth 
cervix.  The  causes  of  the  condition  are  to  be  removed  and  the  patient 
cautioned  to  seek  frequent  dental  attention  as  a  prophylactic  measure. 

Prophylaxis.  As  outhned  above,  the  prevention  of  pyorrhoea  alveo- 
laris  of  the  first  class  involves  the  removal  of  the  local  and,  if  possible, 
the  systemic  causes  of  the  gingivitis,  and  the  systematic  cleansing  of 
the  teeth  at  short  intervals.  The  daily  use  of  the  toothbrush  and 
antiseptic  powders  and  washes  by  the  patient  is  also  important. 

D.  D.  Smith  advises  for  this  class  of  cases  a  thorough  cleansing  once 
a  month,  or  at  first  even  oftener.  The  cleansing  is  to  be  done  with 
an  orange-wood  point,  grasped  in  a  Smith  or  Cogswell  carrier  and 
charged  with  pumice  paste.  The  local  sources  of  gum  infection  are 
thus  continually  removed  and  the  gums  stimulated  by  the  mechanical 
irritation  with  the  wood  point. 

Treatment.  The  treatment  of  well-established  pyorrhoea  alveolaris 
of  the  first  class  is  to  be  considered  under  three  headings:  (1)  the 
removal  of  pus,  calculus,  and  bacterial  films;  (2)  the  prevention  of 
extreme  mobility;  (3)  the  medicinal  treatment  and  the  prophylaxis,  or 
prevention  of  a  relapse  into  the  diseased  condition. 

The  Removal  of  the  Causes.  Calculus  being  an  obvious  irritant 
it  should  be  removed  from  crowais  and  all  parts  of  the  roots.  To 
prevent  infection  of  surrounding  tissues  and  to  remove  the  pus  present 
the  pockets  are  to  be  flushed  out  with  hydrogen  dioxide,  which  may 
be  done  by  means  of  a  syringe  with  fine  nozzle  or  an  atomizer  operated 
by  hand  or  preferably  by  compressed  air.  The  forcible  spray  lifts 
away  the  gum  margin  and  cleanses  the  pockets  mechanically  as  w^ell 
as  chemically.  The  mouth  is  sterilized  at  the  same  time.  If  large 
quantities  of  supragingival  calculus  exist  it  is  well  to  next  remove  the 
gross  deposits  and  permit  the  patient  to  use  an  astringent,  antiseptic 
mouth-wash  for  a  few  days  or  the  operation  may  be  proceeded  with. 

Following  this,  cotton  containing  25  per  cent,  pyrozone  or  10  per 
cent,  trichloracetic  acid  is  to  be  packed  into  the  gum  pockets  in  order 
to  superficially  constringe  the  gum  tissue,  lessen  the  hemorrhage,  and 
render  more  facile  the  removal  of  the  subgingival  calculi.  The  latter 
is  accomplished  with  scalers  of  any  suitable  form.  Those  consisting 
of  flat  blades  to  be  used  with  the  push  cut  are  best  adapted  to  deep- 
seated  calculi,  while  the  more  superficial  deposits  may  be  removed 
with  small,  draw-cutting  excavators. 


PYORRHCEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     559 

Fig.  502  illustrates  the  method  of  guarding  against  unnecessarily 
wounding  the  soft  tissues.  If  the  calculi  be  extraordinarily  inaccessible 
the  pockets  may  be  enlarged  by  packing  for  ten  or  fifteen  minutes  with 
cotton  tampons  saturated  with  the  10  per  cent,  trichloracetic  acid,  which 
also  softens  the  calculi,  or  salicylized  cotton  may  be  left  in  the  pocket 
for  a  day  (Black).     In  some  cases  cocaine  injections  or  applications 

Fig.  502. 


Showing  the  manner  of  holding  an  instrument  for  detaching  calcareous  deposits  when  using 
the  pushing  motion.  The  third  finger  rests  on  the  edges  of  the  teeth,  allowing  freedom  of  the 
hand  to  make  rapid  and  effectual  movements  in  dislodging  the  calculi. 

must  be  made  to  prevent  excessive  pain.  After  removal  of  the  bulk 
of  calculus  with  scalers,  any  fine  granules  or  gummy  collections  may 
well  be  rubbed  off  with  Rhein's  or  coarser  proximal  trimmers,  and  the 
roots  should  then  be  rubbed  with  aromatic  sulphuric  acid  by  the  aid 
of  an  orange-wood  point  mounted  in  a  hand  carrier.  This  is  to  be 
immediately  followed  by  a  syringing  with  bicarbonate  of  soda;  after 
this  medicinal  applications  are  made.     (See  later.)     Good  results  are 


560 


PYORRHCEA  ALVEOLARIS. 


obtained  by  the  use  of  pumice  with  the  stick.  The  scahng  of  each  tooth 
is  to  be  completed  at  one  sitting,  as  repeated  scaUngs  interfere  with  the 
regenerative  process. 

The  gum  margins  are  not  to  be  unnecessarily  wounded,  but  very 
redundant  granulations  may  be  cut  away.    In  cases  of  excessive  loss 


Fig.  503. 


Fig.  504, 


Pyorrhoea  pocket  in  bifurcation. 


The  same  treated  by  scraping  and  filling  with 
gutta-percha.     (Radiographs  by  Price.) 


of  the  pericementum  of  one  root  it  is  well  to  devitalize  the  pulp,  as,  in 
all  probability,  that  organ  will  have  been  overstimulated  and  will  be 
in  a  degenerative  condition,  and  sometimes  is  actually  infected.  An 
abnormal  response  to  thermal  changes   (ordinary  cold)  may  occur 


Fig.  505. 


Heteroplasty  following  the  amputation  of  natural  roots.     (Rheim.) 

(hypersemia  or  inflammation),  or  the  pulp  may  fail  to  respond 'to 
extraordinary  cold  (ethyl  chloride),  indicating  degeneration.  It  has 
been  claimed  by  Rhein,  Smith,  and  others,  that  if  the  pulp  be  devital- 
ized the  nutrition  received  by  it  will  be  diverted  into  the  pericementum 


PYOBRHGEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     561 

to  the  benefit  of  the  latter.  Clinical  experience  seems  to  confirm  this 
statement.  The  method  also  permits  the  use  of  pins  placed  in  the 
root  canal  as  part  of  an  appliance  fixing  the  teeth  in  position.  W.  A. 
Price  recommends  that  an  exposed  pocket  in  the  bifurcation  be  treated 
by  scraping  and  filling  the  same  with  gutta-percha.  If  the  pulp  be 
devitalized  the  bifurcation  may  be  opened  for  the  purpose  of  success- 
fully placing  the  gutta-percha,  which  is  known  to  be  well  tolerated  by 
the  soft  tissues  (Figs.  503  and  504).  In  case  of  hopeless  involvement 
of  one  root  of  a  multirooted  tooth  the  root  may  be  amputated  if  the 
remaining  roots  will  endure  the  strain  put  upon  them.  The  canals  of 
the  roots  retained  must  have  been  previously  carefully  filled. 

Rhein^  calls  attention  to  the  fact  that  collections  are  apt  to  occur 
about  the  surfaces  left  by  the  amputation,  and  that  postextraction 
resorption  of  the  alveolar  process  occurs.  To  obviate  this  he  suggests 
the  use  of  a  porcelain  root  to  replace  the  lost  root,  and  about  which  the 
tissues  contract  firmly  and  remain  in  a  healthy  condition.  This  oper- 
ation Rhein  terms  "  heteroplasty  following  the  amputation  of  natural 
roots." 

Briefly  outlined  the  process  is  as  follows: 

1.  Prepare  and  fill  the  root  canals  as  far  as  the  pulp  chamber;  fill 
this  with  temporary  stopping. 

2.  Amputate  the  necrosed  root  by  means  of  a  fissure  drill,  and 
remove. 

3.  Coat  the  root  with  a  film  of  paraffin  to  allow  for  shrinkage  of 
the  porcelain. 

4.  Take  an  impression  of  one-half  of  the  root  (longitudinally)  by 
embedding  in  plaster;  make  articulating  grooves  and  pour  plaster  for 
an  impression  of  the  other  half;  separate  and  remove  the  root  from 
the  plaster. 

5.  Burnish  matrix  platinum  into  each  half  of  the  impression,  stiffen 
with  porcelain,  and  reburnish.  Complete  one  side  with  porcelain  as  in 
inlay  work,  in  the  other  fuse  a  platinum  box  formed  over  a  square 
platinum  pin  (this  pin  should  be  left  in  the  box  until  the  packing  of 
the  porcelain  about  the  box  is  complete). 

6.  Flatten  the  proximating  sides  of  the  halves ;  paint  with  thin,  fresh 
body;  press  together  and  fuse. 

7.  Strip  off  all  platinum  and  dress  off  all  protruding  points,  coat  the 
entire  porcelain  with  a  thin  film  of  body,  place  in  furnace  in  an  upright 
position,  and  heat  almost  but  not  quite  to  a  glaze. 

1  Dental  Cosmos,  September,  1900,  and  September,  1902. 
36 


562  PYORRHCEA  ALVEOLARIS. 

8.  "Wash  out  socket  of  natural  root  with  antiseptics  and  remove 
temporary  stopping  from  the  crown  cavity;  try  porcelain  root  in  place, 
and  if  right  dry  everything;  fill  the  box  with  cement,  return  the  root 
to  place,  and  pass  the  pin  through  crown  cavity  and  into  the  root 
box.     Adjust  root,  leaving  a  slight  space  for  an  amalgam  joint. 

9.  Pack  the  crown  cavity  and  the  joint  with  amalgam,  and  at  a  later 
sitting  finish  the  same. 

The  Prevention  of  Excessive  IMotion.  The  excessive  move- 
ment of  loosened  teeth  but  increases  the  interstitial  gingivitis  in  the 
remaining  tissues.  These  demand  rest.  Any  excessive  occlusion  due 
to  the  swelling  of  pericemental  tissue  may  be  compensated  for  by 
grinding  the  occluding  surfaces.  Such  excessive  occlusion  and  motion 
are  readily  detected  during  the  act  of  occluding  the  teeth  or  by  means 
of  carbon  paper.  Slightly  loosened  teeth  may  be  temporarily  splinted 
with  ligatures  of  wire  or  floss  silk.    To  prevent  the  slipping  of  these 

Fig.  506.  Fig.  507. 


Diagram  showing  labial  view  of  Mitchell's  Diagram  showing  lingual  view  of  Mitchell's 

spUnt,  with  two  bands  and  wiring.  splint,  with  two  bands  and  bar. 

toward  the  gum  margin  it  has  been  suggested^  that  small  buttons  of 
Harvard  or  other  adhesive  zinc  phosphate  be  placed  upon  the  labial 
faces  of  the  teeth  while  under  the  rubber-dam.  The  floss  silk  may  be 
saturated  with  a  solution  of  chemically  pure  celluloid  in  acetone 
(155  grs.  to  500  grs.)^  to  render  it  impermeable  and  more  lasting.  The 
preparation  after  application  is  allowed  to  dry  under  the  dam  to  a 
coagulum  and  then  dismissed  for  twenty-four  hours,  when  it  may  be 
polished.  It  lasts  for  several  months.  For  certain  cases  Dr.  Hugh 
Mitchell  has  suggested  a  bar  of  iridioplatinum  wdre  adapted  to  the 
lingual  surface  of  the  teeth  to  be  splinted,  and  soldered  to  simple 
gold  bands  to  be  attached  with  cement  to  two  of  the  teeth  adjoining 
the  loose  teeth.  The  other  teeth  are  braced  to  the  splint  with  fine 
wire,  gold  or  platinum  being  preferred  for  anterior  teeth. 

Such  a  splint  may  be  quickly  made  and  is  very  effective,  all  slipping 
of  ligatures  being  prevented;  moreover,  the  wire  may  be  kept  away 
from  the  necks  of  the  teeth  and  the  gums.  After  a  reasonable  period 
of  immobility  the  attachment  secured  by  treatment  may  be  tested  (Figs. 

^  Reitz.  2  Kowarska's  paste 


PYORRHOEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     563 

506  and  507).  Very  loose  teeth  wliich  have  lost  much  of  their  supporting 
alveolar  process  must  be  secured  by  permanent  splints.  The  simplest 
of  these  is  a  series  of  rings  soldered  together  or  its  equivalent,  shown  in 
Fig.  509.  The  teeth  are  firmly  ligated  at  their  necks  with  floss  silk. 
A  wire  measure  is  taken  of  the  entire  circumference  of  the  teeth  to  be 


Fig.  508. 


Fig.  509. 


Temporary  splint  of  silk  floss  or  silver  wire, 
30-gauge  (one  turn  only  shown).  Buttons  of 
zinc  phosphate.     (Rhein.) 


included,  allowance  being  duly  made  for  burnishing.  A  piece  of  thin 
platinum  No.  34  gauge  and  one-eighth  inch  wide  is  cut  to  measure 
and  a  lap  joint  made  and  soldered.  The  ring  is  placed  upon  the  teeth 
and  moulded  to  their  surfaces  and  to  their  interspaces.  The  thinnest 
separating  saw  is  used  to  cut  almost  through  the  splint  on  both  sides 
at  one  interspace.    In  this  groove  a  straight  piece  of  the  platinum  is 


Fig.  510. 


Fig.  511. 


Fig.  512. 


Five  rings  and  included  artificial 
tooth.     (EvansJ 


Two  rings  and  included  arti- 
ficial tooth.     (Evans.) 


Method  of  making  rings 
as  in  Fig.  510.  (Evans.) 


placed  and  the  whole  withdrawn  from  the  teeth  and  the  joints  soldered. 
The  process  is  repeated  at  another  interspace  and  so  on  until  the 
piece  is  complete.  If  the  teeth  are  very  tender  a  plaster  impres- 
sion of  the  tips  of  the  teeth  may  be  taken  and  the  work  done  on  a 
fusible  metal  model.  If  space  be  necessary  the  teeth  may  be  slightly 
disked  upon  their  proximal  sides.  If  such  spacing  be  not  desirable 
the  necessary  room  can  usually  be  obtained  at  the  median  inter- 
space, but  one  platinum  septum  is  placed  and  the  piece  is  to  be 


564  PYORRHCEA  ALVEOLARIS. 

somewhat  stiffened  with  solder  at  the  indentations  representing  the 
interspaces. 

Evans'  method  is  readily  comprehended  by  reference  to  Figs.  510, 
511,  and  512, 

These  splints  are  to  be  cemented  with  adhesive  zinc  phosphate  so 
manipulated  as  to  set  quickly,  and  this  is  best  done  with  the  rubber- 
dam  in  place.    Quick-setting  Harvard  cement  is  excellent. 

The  foregoing  splints  are  too  conspicuous  for  use  in  some 
cases. 

A  simple  device  introduced  by  Dr.  L.  C.  Bryan^  consists  of  a  pure- 
gold  band  about  one-eighth  inch  wide  and  nicely  bevelled  at  its  edges, 
and  is  adapted  about  the  necks  of  the  lower  incisor  teeth  to  be  splinted 
in  somewhat  the  same  manner  that  the  splint  illustrated  in  Fig.  509 
is  adapted.  Particular  attention  is  paid  to  the  interspaces  in  the 
endeavor  to  bring  the  labial  and  lingual  sections  together  at  that  point. 
When  ready  the  piece  is  sprung  off,  the  rubber-dam  is  applied,  zinc 
phosphate  is  placed  ^Hithin  the  band  and  upon  the  necks  of  the  teeth 
at  all  points,  and  the  band  is  put  in  place  and  burnished.  Before  the 
cement  has  set  gold  wire  is  to  be  passed  around  the  interdental  portions, 
tightly  twisted,  and  the  twisted  end  cut  off  to  within  one-eighth  inch 
of  the  band,  and  the  remainder  bent  back  into  the  indentation  in  the 
band.  Dr.  Bryan  recommended  gold  clamps  in  the  place  of  wire, 
but  these  are  difficult  of  adaptation. 

Such  a  piece  is  to  be  placed  only  on  those  lower  incisors  about 
which  salivary  calculus  promptly  collects,  and  should  be  avoided  in 
the  mouths  of  patients  who  will  not  present  frequently  for  prophylactic 
service.  Confined  to  such  cases  they  do  good  service  and  the  cement 
does  not  readily  wash  away;  indeed,  a  slight  coating  of  calculus  seems 
to  protect  the  surface  of  it  from  solution.  If  the  calculus  be  kept  from 
the  gum  margin  this  does  no  harm. 

Several  devices  have  been  offered  which  require  the  devitalization 
of  the  pulps  and  filling  of  the  root  canals  of  the  several  teeth  to  be 
splinted. 

D.  D.  Smith^  suggests  reduction  of  the  Hngual  surfaces  of  the  teeth 
and  the  fitting  to  them  of  thin  metal  backings,  which,  after  adaptation 
to  the  teeth,  are  perforated  and  pins  are  thrust  through  for  the  root 
canals.  After  soldering  each  pin  to  its  plate,  readapting  the  latter 
and  stiffening  with  solder,  an  impression  is  taken  and  the  plates  are 
united.    The  whole  piece  is  cemented  to  place  with  the  rubber-dam 

1  International  Dental  Journal.  1899.  =  Dental  Digest,  1902. 


PYORRHCEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     565 
Fig.  513.  Fro.  514. 


Splint  for  securing  previouslj-  treated  lower 

anterior  teeth.     (Ames,  after  Smith.)  Upper  teeth  prepared  for  splint.     (Ames.' 


Fig.  515. 


Splint  for  use  in  the  case  shown  in  Fig.  514. 
Fig.  516. 


Same  as  Fig.  514.     Splint  in  position. 

Fig.  518.  Fig.  519. 


Tooth  with  Richmond  cap.     (Ames.) 


Fig.  517. 


Root  with  cap  fitted.     (Ames.) 
Fig.  520. 


Splint  for  lower  incisors.     (See  text.) 
(Ames.) 


566 


PYORRHGEA  ALVEOLARIS. 


in  position.     With  this  device  one  or  more  artificial  teeth  may  be 
included  to  replace  lost  incisors  (Figs.  513,  514,  515,  and  516). 

Ames^  suggests  that  in  certain  cases  of  lower  incisors  the  teeth  be 
devitalized  and  amputation  be  performed  at  the  neck  of  each.  Each 
root  is  then  trimmed  and  fitted  with  a  gold  Richmond  cap  without 
pin  (Fig.  517). 


Fig.  521. 


Splint  for  lower  incisors.     (See  text.)     (Ames.^ 
Fig.  522. 


Splint  and  double  saddle  bridge  combined.     ]  roiii  vio\v.     (Ames.) 

Each  natural  crown  is  slightly  trimmed  and  fitted  with  a  gold  Rich- 
mond cap  with  a  pin  (Fig.  518).  These  two  caps  are  united  with  wax, 
carried  to  the  mouth  and  adjusted  in  position.  Each  is  then  carefully 
removed,  the  natural  crown  laid  aside  (in  water),  and  the  gold  sections 
invested  and  soldered  together  (Fig.  519).  The  individual  parts  are 
readjusted  in  the  mouth,  an  impression  taken,  an  investment  made, 

1  Dental  Cosmos,  1903. 


PYORRHCEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     567 

and  all  soldered  together.  The  natural  crowns  are  then  fastened  in 
their  prepared  sockets  with  cement  and  the  piece  is  cemented  to  place. 
Pins  may  be  placed  in  the  roots  if  desired  (Fig.  520). 

If  desired  the  piece  may  be  further  attached  to  the  adjoining  teeth 
by  means  of  the  lingual  plate  and  pin  (Fig.  521).  The  Ames  device 
would  be  useful  in  cases  in  which  proximal  cervical  caries  exists. 

It  may  be  stated  that  three  or  four  teeth  fairly  loose  individually 
when  united  together  may,  as  a  whole,  be  quite  firm. 

Ames  further  suggests  that  in  case  the  pericemental  attachment  is 
hopelessly  lost  such  teeth  may  be  extracted,  the  roots  amputated  and 
prepared  as  for  replantation,  and  then  adjusted  in  the  gold  bridge, 
otherwise  made  as  above  described.     These  roots  are  to  go  in  their 


Fig.  523. 


Fig.  524. 


Right  side  of  extension  bridge,  shown  in 
Fig.  522. 


Left  side  of  extension  bridge,  shown  in 
Fig.  522. 


own  sockets,  and,  being  firmly  fixed  in  position,  the  tissues  settle 
about  them. 

Ames  claims  that  the  extension  bridge  shown  in  Figs.  522,  523,  and 
524  lasted  five  years  and  was  in  as  good  condition  then  as  at  the 
beginning.  Fig.  522  gives  the  anterior  view,  Fig.  523  that  of  the  right 
side,  and  Fig.  524  that  of  the  left  side. 

Rhein  offers  the  following:  After  pulp  removal  and  root  filhng  a 
transverse  groove  is  cut  in  the  lingual  side  of  the  central  or  loose  teeth 
and  a  half-groove  upon  the  mesolingual  aspect  of  the  pier  teeth. 
A  staple  is  formed  of  triangular  iridioplatinum  wire  to  fit  into  the 
root  canals  of  the  pier  teeth.  To  this  is  soldered  a  pin  for  each  of 
the  central  teeth.  The  face  of  the  wire  should  approximately  fit  the 
bottom  of  the  groove.  Rhein  suggests  the  following  method  of  attach- 
ment:   (1)  fill  the  root  with  a  paper  point,  place  cement  over  that,  and 


568 


PYORRHCEA  ALVEOLARIS. 


fill  the  cervical  margin  of  the  cavity  and  its  floor  with  gold ;  (2)  drill 
through  the  gold  to  the  paper  point,  remove  it,  and  refit  the  retaining 
appliance;  when  ready  set  with  zinc  phosphate,  avoiding  excess;  (3) 
when  this  is  set  cut  away  to  the  gold  and  complete  the  gold  fillings. 

A  less  elegant  but  still  practical  method  would  be  to  cover  the  pins 
with  a  good,  color-keeping  amalgam  pressed  into  the  excess  of  cement 
before  it  has  set.  The  margins  are  then  to  be  freed  of  cement  and  the 
operation  completed  with  amalgam,  which  later  should  be  polished. 

Smith's,  Rhein's,  and  Ames'  devices  permit  the  use  of  an  artificial 
tooth  if  necessary.  The  same  may  be  said  for  the  device  which  consists 
of  a  series  of  gold  rings  (Evans'). 

For  the  molars  and  bicuspids  Rhein's  device  is  transferred  to  the 
occlusal  surface  (Fig.  526). 

Short  metal  caps  made  for  the  incisal  tips  of  lower  incisor  teeth 
adjoining  a  space  will  successfully  hold  a  bridge  tooth.  The  device  is, 
however,  rather  conspicuous. 


Fig.  525. 


Fig.  526. 


Permanent  splint  for  cases  of  pyorrhoea  alveo- 
laris  in  upper  or  lower  incisors.     (Rhein.) 


Permanent  splint  for  cases  of  pyorrhcea  alveo- 
laris  on  molars  and  bicuspids. 


For  the  molar  and  bicuspid  teeth  it  seems  good  practice  to  adapt 
short  crowns  to  the  partially  trimmed  teeth  and  unite  these  with 
solder.  A  sort  of  bridge  is  thus  made  which  causes  the  teeth  to  be 
firm  even  if  all  are  originally  loose.  It  is  mainly  this  factor  which 
renders  bridge-work  useful  in  pyorrhoea  alveolaris  upon  isolated  teeth. 

The  use  of  united  barrel  crowns  reaching  the  gum  margins  is  at 
times  useful,  but  the  configuration  of  exposed  roots  may  render  this 
impossible  in  some  cases. 

By  the  use  of  pure-gold  bands,  which  may  be  stiffened  occlusally 
with  solder  to  gain  strength,  better  adaptation  at  cervical  portions  may 
be  obtained  by  hand  burnishing  after  cementation  of  the  piece. 

All  appliances  cemented  to  the  teeth  and  having  a  free  margin  are 
subject  in  some  degree  to  a  solution  of  the  cement.    These  cases  should 


PYOBRHCEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     569 

be  seen  frequently  in  any  event  for  prophylactic  purposes,  when  the 
condition  of  the  appliance  may  be  noted. 

Extraction  and  bridge-work  may  be  at  once  resorted  to  in  some  of 
the  aggravated  cases,  though  if  the  appliance  be  mechanically  con- 
structed teeth  which  may  be  extracted  with  the  fingers  may  be  firmly 
held  in  splints  for  years.  While  this  is  a  fact,  good  judgment  may 
demand  the  early  removal  of  such  teeth  before  an  appliance  is  con- 
structed. 

If  desired  the  bridge  may  be  made  so  as  to  mount  the  natural  teeth 
after  their  extraction,  by  constructing  sockets  of  gold  for  the  reception 
of  the  necks  of  the  teeth  somewhat  after  the  manner  employed  in  the 
Ames  method.  The  sockets  are  then  soldered  to  each  other  and  to 
the  bridge  piers,  after  which  the  teeth  are  attached. 

These  sockets  are  to  be  made  deep  at  first,  and  it  is  well  to  attach 
the  teeth  with  gutta-percha  in  order  that  the  row  of  sockets  or  a  new 
row  may  be  lowered  to  fit  the  gum  if  desirable.  This  will  require  the 
raising  of  the  teeth  to  the  occlusal  level. 

The  Medicinal  Treatment  and  Prophylaxis.  The  pockets  after  scaling 
should  be  forcibly  syringed  or  sprayed  with  hydrogen  dioxide  to 
sterilize  the  pockets  and  remove  particles  of  calculus,  and  then  cau- 
terized with  either  lactic  acid,  full  strength  (Younger);  trichloracetic 
acid,  25  or  50  per  cent,  strength  (Kirk);  or  sulphuric  acid,  25  per 
cent,  strength  (Truman).  If  the  case  be  of  local  origin  the  applica- 
tion of  tincture  of  iodine  to  the  gums  every  other  day  and  the  judicious 
use  of  a  well-made  and  hard  brush  (the  "S.  S.  White  2^,"  "Prophy- 
lactic," "Sanitol,"  or  Talbot's  will  serve)  well  charged  with  an  anti- 
septic and  astringent  tooth-powder,  will  cause  the  gums  to  resorb  to  a 
healthy  consistency. 

Dr.  A.  B.  Harrower  has  suggested  the  following  formula  for  a  powder 
which  has  in  his  own  and  my  hands  given  good  results  as  an  astringent 
antiseptic : 

Jt — Magnesium  carbonate,  lb.  j. 

Cream  of  tartar,  lb.  iss. 

Red  cinchona  bark,  Sij. 

Calcined  alum,  sj. 

Oil  peppermint,  f5v. 

Oil  cinnamon,  f  Siij. 

Oil  rose  geranium,  foj. 

All  ingredients  to  be  finely  powdered.    The  oils  to  be  added  to  the  magnesium  before  thorough 
mixing  of  the  powders.     The  whole  is  to  be  sifted  through  silk. 

Saccharin  may  be  added  to  the  above  as  a  sweetening  agent.     The  powder  when  wet  is  almost 
neutral,  and  should  do  no  harm  in  its  limited  use  as  a  therapeutic  agent. 

Truman  advocates  the  use  of  quinine  sulphate  to  be  packed  in  the 
pockets  as  a  germicide,  and  as  inhibitory  of  diapedesis  of  leukocytes. 


570  PYORRHOEA  ALVEOLARIS. 

Black  has  recommended  the  use  of  the  1-2-3  mixture,  or  phenol- 
camphor,  to  be  put  into  the  pockets  every  three  days,  and  a  few  drops 
to  be  used  on  the  toothbrush. 

K— Oil  of  cinnamon,  1  part. 

Carbolic  acid,  2  parts. 

Oil  of  gaultheria,  3  parts. 

9;— Gum  camphor, 

Crystal  carbolic  acid,  (7a    q.  s. 

Mix  in  a  mortar  to  an  oily  fluid. 

Argyrol,  a  compound  of  metallic  silver,  is  less  irritating  than  silver 
nitrate,  and  may  be  injected  in  25  to  50  per  cent,  aqueous  solution 
with  marked  benefit.    The  application  may  be  made  twice  a  week. 

Regeneration  in  the  pockets  should  not  be  disturbed,  so  that  unless 
the  pus  flow  be  active  one  should  wait  until  sufficient  time  has  been 
afforded  (about  ten  days)  for  granulations  to  form.  If  pus  be  then 
detected  the  pocket  should  be  again  treated  thoroughly.  Good  results 
are  obtained  from  the  use  of  an  astringent  antiseptic  wash  used  in 
forcible  spray  from  an  atomizer.  This  should  be  done  daily  by  the 
patient.  Stagnant  fluids  in  the  pockets  are  washed  out  and  replaced 
by  the  antiseptic,  thus  inhibiting  the  bacterial  growth  in  the  pockets 
and  the  mouth. 

The  teeth  should  be  cleansed  after  meals  to  prevent  media  for 
infection  lodging  about  the  interstices,  after  which  the  antiseptic  spray 
will  aid  in  destroying  bacteria.  The  gums  should  be  massaged  daily 
by  the  thumb  and  forefinger  of  the  patient.  This  strips  the  collec- 
tions from  about  the  gingival  spaces  and  stimulates  a  healthy  cir- 
culation. 

If  the  good  results  of  the  application  of  the  .T-rays  and  high-fre- 
quency currents  claimed  by  C.  H.  Parker,^  W.  K.  Price,  W.  Guy,  and 
others,  shall  be  generally  confirmed,  it  will  be  a  great  aid  in  the  prompt 
reduction  of  this  disease.  It  is  also  possible  that  radium  rays, 
applied  by  radium-chloride-containing  applicators,  or  radio-active 
solutions,  may,  in  the  near  future,  have  a  proven  therapeutic  value. 

The  question  must  be  considered  as  yet  sub  judice.  Good  results 
have  been  obtained  in  some  cases  by  extraction  and  replantation,  after 
root  preparation  and  sterilization  of  the  tooth  and  alveolus.  The 
alveolus  may  have  to  be  deepened. 

If  the  interstitial  gingi^^tis  underlying  the  case  be  of  systemic  origin, 
— i.  e.,  due  to  autointoxication  from  any  disease,  the  alimentary  canal, 

'  Dental  Cosmos,  December,  1903. 


PYORRHOEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS.     571 

the  pyorrhoea  itself,  or  to  drug  action — these  should  have  attention. 
The  systemic  disease  should,  if  possible,  be  cured  by  correct  medical 
attention.  Pyorrhoea  patients  are  of  the  hyperacid  type  (^Michaels) 
and  treatment  should  be  directed  toward  elimination  of  waste  prod- 
ucts and  the  reduction  of  hyperacidity  by  the  use  of  alkaline  rem- 
edies. The  bowels  should  be  kept  active  and  the  skin  pores  open. 
Brisk  exercise  in  the  open  air,  if  not  specifically  contraindicated  by 
organic  disease,  is  valuable  in  both  directions.  Warm  baths  followed 
by  cold  douches  and  vigorous  rubbing  stimulate  the  skin.  Turkish 
baths  followed  by  massage  directed  to  stimulation  of  the  eliminating 
organs  are  valuable  unless  contraindicated.  Free  drinking  of  pure 
water  is  necessary  to  the  successful  elimination  of  the  waste  products 
of  the  body.  The  water  entering  the  blood  increases  the  blood  press- 
ure and  flushes  the  tissues  and  the  kidneys,  dissolving  waste  prod- 
ucts. Water  should  be  freely  taken  between  or  before  meals  in 
order  that  digestion  be  not  interfered  with,  and  if  medicated  with  salts 
of  lithium  the  alkalinizing  effect  and  solvent  action  of  lithium  upon 
urates  are  obtained.  Patients  exhibiting  an  aversion  to  water  drink- 
ing are  more  apt  to  take  it  when  medicated  than  as  a  physiological 
necessity. 

The  prophylaxis  of  pyorrhoea  alveolaris  is  all  important,  especially 
in  the  cases  of  systemic  origin  in  which  chronic  disease  or  malnutrition 
may  not  be  readily  overcome  owing  to  confirmed  habit  of  life  or 
advanced  stage  of  disease.  The  local  conditions  existing  even  after 
a  cure  of  pyorrhoea  are  such  as  to  invite  reinfection  and  the  estabhsh- 
ment  of  microbic  plaques,  which  frequent  cleansing  of  the  teeth  vnW 
remove.  The  system  of  monthly  or,  if  necessary,  more  frequent 
cleansing  advocated  by  D.  D.  Smith  should  be  practised.  Its  good 
results  are  particularly  manifest  in  this  class  of  cases. 

Recurrence  of  the  condition  is  probable  if  the  oral  prophylaxis  or 
systemic  treatment  be  neglected.  The  simpler  cases  yield  quite  readily; 
the  advanced  ones,  in  which  much  of  the  alveolar  process  is  lost,  tax 
the  patience  of  operator  and  patient  alike,  and  are  apt  to  end,  sooner 
or  later,  in  loss  of  the  teeth  affected. 

This  fact,  however,  should  not  prevent  the  retention  of  these  teeth 
by  every  means  at  command  during  the  period  for  which  they  may 
be  made  useful.  If,  however,  any  tooth  prove  an  incurable  source  of 
pus  formation  it  should  be  removed,  otherwise  the  remaining  teeth 
are  continuously  infected. 


572  PYORRHCEA  ALVEOLARIS. 

SYSTEMIC   EFFECTS   OF   PYORRHCEA   ALVEOLARIS. 

It  has  been  abundantly  shown  by  Hunter  and  others  that  the  pus 
of  pyorrhoea  and  other  intense  oral  sepsis  is  a  source  of  systemic 
infection,  producing  effects  ranging  from  gastritis  to  actual  septic 
infection.  The  importance  of  this  fact  is  not  to  be  lost  sight  of,  and 
patients  are  to  be  informed  of  the  dangers  of  constant  pus  formation, 
as  well  as  of  the  presence  of  other  forms  of  sepsis  about  the  mouth 
and  teeth. 

Goadby^  reports  the  cure  of  a  case  of  profound  muscular  weakness, 
mental  depression,  and  insomnia  after  unavailing  general  medical  treat- 
ment for  neurasthenia,  as  following  the  extraction  of  teeth  affected  by 
pyorrhoea. 

Hunter  and  Leith"  have  described  cases  of  subacute  and  chronic 
catarrh  of  the  stomach  and  phlegmonous  gastritis  due  to  the  ordinary 
pyogenic  cocci,  such  as  are  found  in  the  mouth,  and  which  the  gastric 
juice  of  the  stomach  of  the  particular  individual  at  least  was  not 
competent  to  kill.  Considering  the  fact  that  an  oral  subacute  catarrhal 
condition  is  established  in  pyorrhoea,  the  local  transfer  of  the  infection 
is  not  surprising. 

D.  D.  Smith^  claims  to  have  cured  cases  of  confirmed  nervous 
dyspepsia,  nervous  prostration,  and  other  local  and  systemic  conditions 
simply  through  constant  dental  prophylaxis. 


PYORRHCEA  ALVEOLARIS  NOT  DEPENDENT  UPON  CALCULUS 

FORMATION. 

Phagedenic  Pericementitis.  By  the  term  phagedenic  pericemen- 
titis Black  has  distinguished  a  form  of  interstitial  gingivitis,  the  chief 
characteristics  of  which  are  the  more  or  less  rapid  destruction  of  a  por- 
tion of  the  pericementum  and  the  resorption  of  the  alveolar  process 
contiguous  to  the  lost  area;  leaving  a  pocket  extending  from  the  gum 
margin  which  may  be  partly  intact  to  a  point  deep  in  the  alveolus,  and 
from  which  much  or  little  pus  may  exude.  The  disease  may  be  con- 
sidered under  the  heading  of  pyorrhoea  alveolaris,  beginning  with  a 
marginal  gingivitis,  but  of  aggravated  type  and  especially  virulent 
infection. 

^  International  Dental  Journal,  July,  1902. 

*  Transactions  Odontological  Society  of  Great  Britain,  International  Dental  Journal,  1899. 

3  Proceedings  Philadelphia  County  Medical  Society,  1903. 


PHAGEDENIC  PERICEMENTITIS.  573 

Whatever  its  cause  the  disease  presents  a  peculiar  rate  and  manner 
of  progress  which  warrant  a  special  description. 

Causes.  The  causes  of  this  condition  seem  to  be  clearly  infective, 
the  evidence  of  this  being  the  fact  that  it  yields  only  to  operation  for 
removal  of  infected  tissue  or  infective  material,  and  to  the  action  of 
germicides.  Without  doubt  systemic  conditions  favoring  tissue 
debility  may  act  as  predisposing  causes.  A  proportion  of  the  cases 
begin  with  a  marginal  inflammation  of  acute  form,  sometimes  asso- 
ciated with  calculus  formation  and  sometimes  without  it.  In  several 
cases  observed  some  form  of  traumatism,  such  as  violent  and  per- 
sistent wedging,  blows,  etc.,  or  malocclusion,  has  preceded  the  develop- 
ment of  the  disease.  The  infection  usually  spreads  from  one  tooth 
to  another ;  in  other  cases  one  or  two  teeth  may  be  the  only  ones  affected. 

Black  failed  to  find  any  association  of  this  condition  with  gout, 
rheumatism,  or  heredity,  but  considered  the  scrofulous  diathesis  and 
anaemia  as  general  predisponents.  He  considers  the  deposition  of 
calculus,  if  present,  as  favoring  the  action  of  the  infecting  fungus,  and 
that  the  latter  is  peculiar  and  of  virulent  type,  though  the  specific 
fungus  was  not  established. 

He  views  it  as  an  oral  fungus  not  subject  to  technical  methods  of 
cultivation  and  study  as  yet  developed  by  bacteriologists.  He  regards 
the  pericemental  glands  as  the  avenues  by  which  infection  travels 
from  the  gingival  space  into  the  deeper  portions  of  the  pericementum. 

Pathology.  The  disease  begins  with  a  marginal  infection  which 
infiames  the  pericemental  margin.  The  infection  advances  toward 
the  apex  of  the  root,  either  slowly  or  rapidly,  and  following  often  but 
one  side  of  the  root.  The  pericementum  is  liquefied,  the  alveolar 
process  disappears  by  resorption,  and  a  distinct  pocket  is  formed. 
The  gum  may  be  partly  resorbed  from  about  the  neck  of  the  tooth, 
but  need  not  be  markedly  destroyed. 

Hyperostosis  of  the  outer  edge  of  the  alveolar  process  may  occur 
(Fig.  497),  or  the  process  may  disappear  at  this  point.  When  the 
infiammation  of  the  pericementum  is  deeply  established  the  tooth 
involved  may  shift  its  position  laterally,  carrying  another  tooth  with 
it,  and  elongate  far  beyond  its  fellows,  sometimes  establishing  mal- 
occlusion, but  sometimes  the  teeth  are  not  in  occlusion  at  all.  Black 
considers  this  due  to  the  pressure  produced  by  the  swelling  of  the 
inflamed  pericementum. 

The  advance  of  the  disease  toward  the  apex  may  be  very  rapid, 
the  pericementum  being  destroyed  even  over  the  apex  of  the  root,  or 


574  PYORRHCEA  ALVEOLARIS. 

of  one  root,  while  the  attachment  upon  the  other  side  of  the  tooth 
may  hold  it  in  position. 

Black  regards  the  absence  of  decided  mobility  of  the  tooth,  even 
though  sliortlv  after  the  tooth  may  drop  out,  as  characteristic  of  this 
condition. 

Examination  of  the  area  of  the  root  involved  usually  demonstrates 
either  calculi  or  a  substance  of  viscous  nature  or  both  attached  to 
its  surface.  Pus  may  exude  in  some  quantity  from  the  gum  margin, 
but  it  may  not  be  of  great  amount.  .  Of  course  the  pocket  may  afford 
ingress  to  the  ordinary  pyogenic  organisms  of  the  mouth,  which  may 
not  be  the  primary  cause  of  the  disease,  but  merely  implanted  upon  a 
favoring  soil.  The  calculus  present  may  be  a  deposit  from  this  pus 
or  from  the  serum  exuded  bv  the  inflamed  tissue. 


Fig.  527 


Phagedenic  pericementitis.  Pockets  as  shown.  Teeth  were  one-sixteenth  inch  longer,  but 
have  been  shortened.  Practically  no  calculus  and  but  slight  flow  of  thick,  creamy  pus.  Gum 
prominent  over  affected  teeth. 

The  advance  of  the  case  may  be  very  slow  and  limited  to  the  teeth 
originally  involved.    The  following  is  an  example: 

Miss  H.,  aged  twenty-five  years,  presented  with  well-established 
pockets,  extending  one-half  inch  toward  the  apex,  upon  the  mesal 
aspect  of  the  root  of  the  right  upper  central  incisor  and  distal  and 
distobuccal  aspect  of  the  right  upper  lateral  incisor.  There  was  a 
history  of  traumatism  due  to  violent  and  persistent  wedging  wdth 
rubber  at  about  the  age  of  sixteen.  The  case  was  then  of  several 
years'  standing  and  the  two  teeth  elongated  about  one-eighth  inch 
beyond  their  fellows  (Fig.  527).  The  pockets  were  treated  with 
some  benefit  and  the  teeth  shortened  for  the  cosmetic  efi'ect,  but  the 
patient  left  the  city  suddenly  before  recovery,  and  was  not  seen  again 
for  three  years.     At  this  second  visit  it  was  found  that  the  pockets 


PHAGEDENIC  PERICEMENTITIS. 


575 


Fig.  528. 


were  nearly  the  same  as  at  first  and    no  other  teeth  had    become 
involved.     Nor  had  the  teeth  further  elongated. 

The  destruction  of  the  tissues  may  assume  several  forms.  In  certain 
mouths,  especially  in  neurasthenic  and  aneemic  patients,  a  ^iscous 
material  may  accumulate  upon  the 
necks  of  teeth  or  exposed  roots;  and 
the  pericementum,  bone,  and  gum  may 
rapidly  inflame  and  disappear,  leaving 
the  roots  exposed  to  collect  more  of  the 
material. 

The  resorption  may  occur  as  shown 
in  Fig.  529,  or  the  gum  may  be  split 
and  the  destruction  follow  the  length 
of  the  root  on  one  side  only  until  even 
the  apex  is  reached  (Fig.  528). 

The  tooth  may  be  loose  or  firmly  attached  by  the  remainder  of  the 
pericementum. 

Fig.  529  is  a  model  of  the  lingual  side  of  the  right  upper  teeth  under- 
going the  former  process.  The  left  upper  posterior  teeth  and  the  lower 
incisors  have  also  been  lingually  affected.  There  is  but  little  calculus, 
but  the  viscous  material  is  quite  abundant,  black  stain  is  present,  and 
dental  caries  is  rife.    The  patient  has  been  anaemic  and  neurasthenic 


Destruction  of  pericementum,  bone,  and 
gum  over  buccal  root  of  a  molar. 


Fig.  529. 


Resorption  of  gum  over  palatal  root  of  an  upper  molar,  associated  with  but  trifling  deposit  of 
calculus,  but  the  root  is  covered  with  a  viscid  deposit.  Age  thirty-two  years.  Patient  neuras- 
thenic and  of  tuberculous  diathesis. 


for  years,  and  one  lower  molar  has  been  removed  for  resorption  of  the 
apices  of  the  roots  associated  with  looseness. 

When  pericemental  destruction  has  involved  the  apical  pericementum 
death  of  the  pulp  occurs,  and  infection  of  the  necrosed  pulp  results; 
abscess  forms  and  pus  discharges  via  the  pyorrhoea  pocket. 


576     ■  PYORRHCEA  ALVEOLARIS. 

\Mien  the  disease  attacks  but  one  root  of  a  molar,  destruction  of  the 
pericementum  around  that  root,  death  of  half  of  the  pulp,  and  abscess 
formation  may  result,  and  the  other  roots  be  unaffected;  a  portion  of 
the  pulp  of  the  tooth  may  retain  its  vitality  for  some  time,  notwithstand- 
ing the  apical  abscess  upon  one  root.  In  these  cases  pus  discharge 
from  about  the  root  of  a  tooth  may  be  continued. 

A  form  of  phagedenic  pericementitis  causing  very  rapid  destruction 
of  the  pericementum  and  loss  of  the  teeth  without  loss  of  alveolar  wall 
has  occasionally  been  noted.  In  one  notable  case  two  upper  incisors 
came  away  three  weeks  after  an  ulceration  appeared  about  their  gum 
margins.  The  patient  wore  the  teeth  for  several  weeks  in  situ,  and 
could  remove  and  reinsert  them  at  will.  The  alveolar  walls  were  bare, 
but  intact.  There  was  but  little  pain.  The  sockets  healed  after  re- 
moval of  the  teeth  and  the  freshening  of  the  bone.  While  perhaps 
classifiable  under  this  heading,  the  clinical  features  of  this  case  were 
entirely  distinct  from  those  of  the  phagedenic  condition  recognized  as 
phagedenic  pericementitis,  and  were  more  probably  caused  by  the 
so-called  stomatitis  ulcerosa. 

The  acute  gingival  abscess  sometimes  noted  in  connection  with 
pyorrhoea  alveolaris,  and  secondary  to  it,  may  sometimes  occur  in 
connection  with  this  condition  (Fig.  500). 

While  the  disease  is  usually  first  noted  about  a  single  tooth,  it  is 
rare  that  a  lengthened  period  elapses  before  it  makes  its  appearance 
about  other  teeth;  usually  an  adjoining  tooth  or,  it  may  be,  on  a  distant 
one.  This  disease  may  make  its  appearance  in  the  mouths  of  patients 
who  take  extraordinary  care  of  the  teeth,  in  mouths  where  the  teeth 
are  apparently  entirely  free  from  deposits,  where  the  gum  appears 
normal,  and  where  the  teeth  are  free  from  caries.  It  is  of  more  frequent 
occurrence  in  dentures  comparatively  free  from  caries  than  in  those 
where  caries  prevails  or  has  prevailed. 

Symptoms  and  Diagnosis.  The  disease  being  often  of  rapid  onset, 
nothing  may  be  noted  until  the  patient  complains  of  pain  about  the 
teeth,  when  the  pocket  may  be  found  as  described.  A  hne  of  deepened 
color  in  the  gum  over  the  pocket  may  also  be  noted.  The  shifting  of 
teeth  points  to  the  condition;  otherwise  the  signs  noted  under  the 
pathology  are  the  distinguishing  characteristics. 

A  differential  diagnosis  may  have  to  be  made  between  phagedenic 
pericementitis  in  its  later  stages  and  acute  apical  abscess  or  peri- 
cemental abscess. 

Thermal   or  electric   tests,  or   a    history  of   response   to  thermal 


PHAGEDENIC  PERICEMENTUM.  577 

changes,  may  indicate  at  least  partial  vitality  of  the  pulp  which  may 
have  undergone  degeneration.  Any  excessive  response  not  reduced 
by  treatment  of  the  pyorrhceal  condition  and  any  lack  of  response 
to  decided  thermal  or  electric  tests  indicate  pulp  inflammation  or 
degeneration  and  a  necessity  for  pulp  devitalization. 

Prognosis.  The  prognosis  of  this  disease,  so  far  as  the  teeth  affected 
are  concerned,  is  in  general  decidedly  unfavorable.  While  it  may  be 
temporarily  arrested  in  its  earlier  stages,  its  recurrence  and  ultimate 
loss  of  the  affected  teeth  are  the  rule.  It  may  attack  but  few  teeth  of 
a  denture  and  progress  until  they  are  lost,  the  other  teeth  remaining 
unaffected.  The  common  history,  however,  is  that  when  the  disease 
makes  its  appearance  the  denture  is  ultimately  lost  through  it,  although 
the  period  of  loss  may  cover  many  years.  Several  years  may  elapse 
between  the  loss  of  one  tooth  and  the  affection  of  the  second.  Upper 
incisors  and  molars  appear  to  suffer  more  frequently  from  the  disease 
than  any  of  the  other  teeth. 

Treatment.  It  has  been  asserted^  that  if  in  the  early  stages — i.  e., 
that  of  tooth  shifting — the  pulp  be  removed  and  the  canal  filled,  the 
impending  degeneration  and  necrosis  of  the  pericementum  will  be 
averted.  The  probable  explanation  is  that  the  diversion  of  the  blood 
stream  of  the  pulp  into  the  pericemental  vessels  enlarges  them  in 
compensation  of  a  degree  of  endarteritis  obliterans  produced  by  the 
interstitial  gingivitis.  Possibly  the  extra  nutrition  thus  obtained  by 
the  pericementum  fortifies  it  against  degenerative  changes,  and  possibly 
even  against  the  existing  infection. 

The  treatment,  as  regards  splinting  of  the  teeth  and  sterilization  of 
the  pockets,  is  the  same  as  in  the  first  class.  Black  emphasizes  two 
points  of  much  importance  in  the  next  stage  of  treatment — i.  e.,  the 
removal  of  deposits — first,  that  the  gum  margin  must  not  be  unneces- 
sarily injured;  secondly,  that  vigorous  scaling  of  the  roots  may  be 
done  without  special  regard  to  avoid  cutting  the  tissues  lining  the 
pocket,  instead  of  avoiding  such  injury,  as  in  the  first  class  of  pyorrhoea. 
The  pockets  are  freely  syringed  with  hydrogen  dioxide,  or  with  a 
1 :  500  solution  of  mercuric  chloride  in  hydrogen  dioxide.  The  alveolar 
edges  are  to  be  freely  scraped  with  the  scaling  instruments,  which 
should  have  slender  stems  and  comparatively  broad  cutting-blades 
(Fig.  530).  The  use  of  cauterants,  such  as  trichloracetic  and  lactic 
acids,  is  more  important  than  in  the  former  type  of  disease.  The  same 
astringent  antiseptic  washes  are  to  be  prescribed.    After  removing  all 

1  M.  L.  Rhein.D.  D   Smith. 
37 


578 


PYORRHCEA  ALVEOLARIS. 


foreign  material,  including  dead  matter  and  sterilizing,  correcting 
occlusion,  and  securing  immobility,  the  astringent  antiseptic  wash  is 
expected  to  draw  the  tissues  tightly  about  the  teeth  and  to  prevent 
infection,  so  that  a  regenerative  process  can  be  established  in  the  vital 
tissues  of  the  former  disease  pocket. 

In  case  the  pockets  are  so  deep  or  have  such  form  that  the  alveolar 
margins  cannot  be  well  trimmed  without  overstretching  or  injuring  the 
gingival  edges.  Black  advises  that  gum  flaps  be  raised,  exposing  the 
alveolar  margins  (Fig.  531).  A  semicircular  incision  is  made  and 
turned  back,  and  bleeding  checked.  By  means  of  sharp  chisels  the 
alveolar  borders  are  freely  scraped,  the  pockets  are  flushed  with 
hydrogen  dioxide,  and  the  flap  secured  by  a  couple  of  stitches.  Cocaine 
anaesthesia  should  precede  this  operation.  The  sa,me  writer  advises, 
in  cases  where  eversion  of  the  alveolar  margin  has  occurred,  that  the 


Fig.  530. 


Fig.  531. 


Scalers  (three  times  natural  size). 


Illustration  of  the  position  and  form  of  incision  through 
the  gum  for  exposing  the  root  of  the  tooth  and  injured 
alveolar  process  :  a,  incision.     (Black.) 


process  be  exposed  by  cuts  and  broken  down  by  three  cuts  made  with 
a  sharp  chisel  and  mallet;  the  loosened  segment  of  bone  to  be  pressed 
firmly  against  the  root.  It  is  desired  next  that  the  entire  pocket  will 
fill  with  granulation  tissue,  and  organization  of  the  granulations  take 
place,  furnishing  reattachment.  That  this  occurs  in  some  cases  is 
undoubted.  Black  believes  that  a  reproduction  of  alveolar  margins 
also  occurs  in  some  cases.  The  hope  of  good  results  lies  in  keeping 
the  parts  aseptic  after  all  foreign  deposits  and  dead  material  have 
been  removed. 

For  this  purpose  the  case  should  be  seen  every  few  days  while  under 
treatment,  so  that  the  pockets  may  be  injected  with  antiseptic  sub- 
stances, such  as  1-2-3  mixture  or  phenol-camphor. 

Particular  attention  should  be  paid  to  the  prophylactic  treatment. 


CHAPTER   XXVI. 

PERICEMENTAL   ABSCESS. 

In  comparatively  rare  cases  there  begins  in  the  lateral  aspect  of  a 
pericementum  a  swelling  which  finally  discharges  its  contents  either 
at  the  gum  margin  or  directly  through  the  gum  tissue. 

The  pulp  of  the  tooth  may  be  perfectly  vital  and  the  attachment  at 
the  gum  margin  at  first  at  least  practically  unbroken.  A  deposit  of 
calculus  may  or  may  not  be  formed  in  the  area,  and  the  discharge  may 
consist  of  a  glairy  mucus  or  of  purulent  matter.  Cases  of  this 
disease  have  been  noted  and  described  by  Darby  (1874),  W.  E.  Walker 
(1895),  D.  D.  Smith  (1897),  and  Kirk^  (1898). 

Causes  and  Pathology.  When  seen  as  above  described  the  condition 
occurs  in  the  mouths  of  individuals  predisposed  to  pyorrhoea  alveolaris 
associated  with  general  malnutrition^ — i.  e.,  there  is  an  interstitial 
gingivitis  present  in  the  area  affected  that  may  be  predisposed  to  by 
an  autointoxication,  the  result  of  a  general  malnutrition  or  intestinal 
toxaemia.  The  general  association  of  malnutritional  conditions  with 
an  excess  of  waste  products  in  the  blood  leads  to  the  just  inference 
that  such  waste  floating  through  the  tissues  acts  as  an  irritant,  lessening 
in  time  the  vital  energy  of  the  cells  of  a  part  or  of  the  body  as  a  whole. 
For  this  reason  gout  and  kindred  diseases  are  considered  at  least 
predisposing  causes  of  pericemental  abscess  and  pyorrhoea  alveolaris. 

The  frequent  association  of  malnutritional  conditions  with  an  excess 
of  uric  acid  in  the  blood  in  the  form  of  its  urates,  and  the  demon- 
stration by  C.  N.  Peirce,  in  1892,  that  such  urates  exist  in  the  deposits 
upon  the  lateral  aspect  of  the  tooth  affected,  gave  force  to  his  claim 
that  uric  acid  or  the  waste  products  associated  with  it  are  responsible 
for  the  concretions  and  the  symptoms. 

E.  T.  Darby  (1880),  W.  J.  Reese  (1886),  and  J.  S.  Marshall  (1891) 
pointed  out  the  relation  of  gout  with  certain  pericemental  conditions. 

Kirk's  studies  in  pericemental  abscess  have  demonstrated  that  in 
a  few  cases  the  diplococcus  pneumoniae  may  be  found  in  pure  culture 
in  the  abscess  when  first  opened.  The  question  still  sub  judice  is:  (1) 
whether  the  toxic  waste  products  floating  in  the  sluggish  blood  stream 

1  Dental  Cosmos,  1898  and  1901.  -  E.  C.  Kirk,  Dental  Cosmos,  November,  1900. 


580  PERICEMENTAL  ABSCESS. 

of  the  affected  portion  of  the  pericementum  cause  interstitial  gingivitis, 
and  a  necrotic  area  from  which  the  degenerated  tissue  and  coagulated 
lymph  are  expelled  as  the  contents  of  a  gouty  abscess ;  or  (2)  whether 
the  diplococcus  pneumoniae  or  some  other  organism  enters  an  area 
irritated  by  the  waste  products,  etc.,  and  excites  the  acute  conditions 
— such  organisms  have  two  possible  avenues  of  entrance  to  the  diseased 
area:  (a)  via  the  general  circulation;  (b)  from  the  gingival  space  via 
the  pericemental  glands  of  Black  or  the  bloodvessels;  or  (3)  whether 
the  said  organisms  are  alone  capable  of  exciting  the  disease  as  a  purely 
local  phenomenon. 

The  association  of  gout  with  at  least  a  proportion  of  the  cases 
requires  a  consideration  of  its  pathology,  which  will  serve  to  illustrate 
the  principle  of  autointoxication.     (See  also  interstitial  gingivitis.) 

General  Pathology.  The  conditions  called  gouty  are  held  to  be  due 
to  the  retention  in  the  circulating  fluids  of  an  excess  of  urates,  a  waste 
product  of  tissue  and  food  metabolism;  this  excess  of  material  acts 
as  an  irritant  and  inflammation-exciting  agent  in  the  tissues  of  the 
body,  producing  alterations  of  function  and  structure  in  many  tissues 
and  organs,  but  most  palpably  in  the  members  of  the  connective-tissue 
group.  The  association  of  an  excess  of  urates  with  gout  was  demon- 
strated by  Garrod,  who  detected  crystals  of  urates  in  the  serum  of 
blisters  from  gouty  patients.  The  association  became  still  more  clear 
after  an  examination  of  the  calculi  of  gout,  which  were  found  to 
contain  urates.  In  gouty  joint  affections  urates  of  sodium  are  found 
in  the  diseased  areas,  and  they  constitute  the  common  tophus  found 
in  gouty  patients. 

Urates  of  sodium  are  also  discharged  in  gouty  abscesses  tlirough  the 
skin,  either  in  liquid  or  solid  form,  and  with  or  without  pus  (Musser). 

According  to  Musser^  a  number  of  these  abscesses  may  discharge 
without  impairment  of  the  general  health,  or  even  with  benefit  to  the 
system. 

It  is  demonstrable  that  the  deposition  of  crystals  of  sodium  biurate 
in  and  about  joints  are  the  cause  of  acute  but  non-suppurative  inflam- 
mations of  those  joints.  The  conditions  necessary  for  deposition  seem 
to  be  a  sluggish  circulation  in  the  part  which  permits  the  urates  to 
infiltrate  into  and  crystallize  in  tissues  somewhat  degenerated  by  the 
sluggish  cu-culation  and  consequent  deficient  oxidation.     (See  p.  66.) 

In  gouty  patients  there  is  a  tendency  to  degenerative  changes,  prob- 
ably induced  in  parts  by  the  irritative  effects  of  the  urates  before 

^  Medical  Diagnosis. 


PERICEMENTAL  ABSCESS. 


581 


Fig.  532. 


deposition  in  quantity.  There  is  first  a  tendency  to  sclerosis — i.  e.,  to 
the  development  of  the  connective  tissues  at  the  expense  of  the  cellular 
elements  peculiar  to  the  parts. 

Gout,  or  uric  acid  poisoning,  may  exist  as  a  chronic  affection  without 
acute  outbreaks;  deposits  accumulate  in  small  joints  (tophi),  as  of 
the  fingers,  causing  stiffness  and  deformity,  as  the  joints  are  succes- 
sively affected.  An  injury  to  a  joint  may  determine  the  affection  in 
that  joint,  and  any  joint  may  be  affected  (Fhnt).     (Fig.  532.) 

Gout  may  exist  as  an  obscure  affection  without  any  of  the  joint 
affections  noted.  Tophi  may  deposit  in  tendons  (Ziegler) .  Disorders 
of  the  stomach,  liver,  kidneys,  heart, 
bloodvessels,  and  lungs  may  all  at- 
tend chronic  gout,  and  be  caused 
by  it.  The  evidence  of  connection 
of  obscure  conditions,  such  as  head- 
ache, hebetude  of  mind,  lassitude; 
digestive,  circulatory,  or  respiratory 
troubles,  with  the  gouty  condition, 
may  only  be  made  manifest  by  their 
relief  through  antigout  therapeusis. 

All  forms  of  gout  are  largely  he- 
reditary. The  manifestation  of  the 
diathesis  may  skip  one  generation 
and  appear  in  the  next.  Hereditary 
gout  in  the  female  may  manifest 
itself  as  rheumatoid  arthritis.  In 
a  proportion  of  cases  no  heredity 
can  be  traced,  although  the  exist- 
ence of  gout  in  the  individual  is 
unmistakable.  The  deposits  in  gout  are  only  readily  detected  when 
they  exist  as  defined  concretions.  They  may  be  present  as  fine  crystals 
and  escape  detection. 

The  chief  causes  of  a  rise  of  uric  acid  in  the  blood  are:  (1)  diseases 
or  conditions  in  which  oxidation  of  waste  products  is  lessened — 
e.  g.,  anaemia,  sedentary  life  or  occupation;  (2)  a  diet  introducing 
albuminous  or  starchy  and  perhaps  inorganic  constituents  in  excess 
of  the  ability  of  the  tissues  to  appropriate  or  oxidize  the  resulting 
products,  or  which  disturb  the  alimentary  and  hepatic  functions;  (3)  a 
lessened  elimination  of  waste  products,  normal  or  otherwise,  from  the 
system. 


Tophi  of  gout.    (Ziegler.) 


582  PERICEMENTAL  ABSCESS. 

Heredity,  age,  and  habits  of  life  are  all  contributory  to  the  above. 

Special  Pathology.  The  test  of  the  soundness  of  the  theory  that  there 
are  distinctive  gouty  dental  affections  depends  upon  whether  their 
causation,  pathology,  and  symptoms  are  explainable  by  the  phenomena 
of  gout  exhibited  in  other  parts,  and,  again,  by  the  effects  of  antigout 
therapeusis. 

First,  an  examination  of  the  teeth  themselves.  Upon  section  the 
enamel,  dentine,  and  cementum  of  the  teeth  lost  by  this  disease  are 
found  to  be  highly  organized.  The  pulp  chambers  are  frequently 
almost  obliterated,  even  without  external  evidences  of  abrasion  or 
erosion.  Data  relative  to  the  condition  of  the  pulp  and  pericementum 
are  wanting,  although  from  the  degree  of  immobility  of  the  teeth  it 
may  be  inferred  that  the  pericementum  is  markedly  diminished  in 
volume  prior  to  the  beginning  of  the  disease. 

These  facts  indicate  an  increase  in  the  intercellular  elements  of  the 
parts,  at  the  expense  of  the  essential  cellular  elements  (sclerosis),  as 
a  result  of  a  chronic  irritation. 

The  articulation  of  the  teeth  with  the  maxillse  is  by  implantation  in 
alveoli  (gomphosis),  relation  being  secured  by  the  fibrous  membrane 
— the  pericementum.  While  not  a  joint  in  the  ordinary  sense,  it  may 
be  practically  viewed  as  such.  There  is  no  reason  why  under  certain 
favoring  conditions  urates  may  not  be  deposited  in  the  pericementum 
as  well  as  in  the  metatarsophalangeal  joint  or  in  the  joints  of  the 
fingers  or  the  knee.  Reference  to  Fig.  532  will  demonstrate  that  the 
deposit  may  occur  in  white  fibrous  tissue,  such  as  tendons  (Ziegler) . 
That  the  deposit  of  urate  may  be  slight  and  masked  by  subsequent 
deposits  of  calcium  phosphate  does  not  imply  more  than  that  the 
peculiarity  of  the  tissue  may  produce  a  peculiar  deposit. 

It  is  probable  that  the  hyperaesthesia  about  the  teeth,  accompanied 
by  a  disposition  to  grind  the  teeth  at  night,  and  a  disposition  to  shifting 
of  positions  of  the  teeth  are  explainable  upon  the  ground  of  general 
irritation  of  the  pericementum  as  the  result  of  the  presence  in  them 
of  an  excess  of  urates. 

An  outbreak  of  the  acute  form  of  gouty  pericementitis  upon  some 
one  tooth  is  explainable  by  the  fact  that  an  area  of  debility  has  been 
established  upon  the  said  tooth  by  some  local  cause,  such  as  overuse, 
malocclusion,  disuse,  abuse,  chance  blows,  etc.  The  sluggish  circula- 
tion estabhshed  in  the  area  causes  the  deposition  of  urates  to  occur 
in  the  degenerative  tissue  of  the  area.  (See  calcareous  degenera- 
tion.) 


•    PERICEMENTAL  ABSCESS.  583 

Inflammation  of  a  chronic  or  acute  nature  is  excited  and  pyogenic 
infection  may  or  may  not  occur,  either  by  way  of  the  circulation  or 
from  the  gum  margin  by  way  of  the  pericemental  glands  of  Black. 

Teeth  have  been  extracted  during  this  period,  one  of  which  exhibited 
these  significant  features:  The  apical  pericementum  was  intact,  as 
was  also  that  portion  toward  the  gingival  margin;  between  the  two 
was  an  area  of  denudation  in  which  loosely  attached  to  the  root  was 
a  rough,  irregular  calculus  (Burchard). 

Calculi  scraped  from  the  roots  of  such  teeth  exhibit  in  a  varying 
degree  a  response  to  the  murexid  test,  the  test  for  urates  (Peirce). 
The  reaction  may  be  very  faint  in  some  cases,  being  overshadowed  by 
the  calcium  phosphate  which  makes  up  the  bulk  of  these  masses;  in 
others  it  is  pronounced — i.  e.,  urates  make  up  a  portion  of  the  deposits. 

Fig.  534. 


A  and  C,  vital  pericementum;  B,  gouty  calculus  ;  A,  calculus  in  area  of  necrosis;  B  and 

D,  a  subgingival  calculus.  C,  -idtal  pericementum. 

Black^  by  test  found  urates  in  nearly  all  concretions,  salivary  and 
serumal,  about  the  teeth.  While  he  claimed  that  this  proved  that 
urates  have  no  causal  relation  to  pyorrhoea,  the  findings  seem  rather 
to  point  to  frequent  presence  of  urates  in  the  salivary  and  serumal 
excretions,  which  may  really  be  a  cause  of  irritation  even  when  no 
obvious  symptoms  of  gout  are  present. 

Miller's  demonstration  of  a  calculus  upon  an  unerupted  tooth  is  to 
be  recalled.     (See  p.  549.) 

Other  cases  have  occurred  in  which  no  calculus  was  present,  but  a 
small  sac  was  found  in  the  pericementum,  either  at  the  lateral  aspect 
or  in  the  bifurcation.  This  sac  may  contain  a  globule  of  pus  (D.  D. 
Smith). ^ 

If  a  collection  of  fluid  form  and  discharge  the  condition  is  known 

1  Dental  Review,  1894.  -  Dental  Cosmos,  1897. 


534  PERICEMENTAL  ABSCESS. 

as  a  gouty  abscess  or,  as  more  lately  termed,  a  pericemental  abscess. 
The  fluid  may  consist  of  coagulated  lymph  or  of  pus.  The  discharge 
in  the  one  case  may  be  glairy,  in  the  other  purulent. 

If  the  abscess  be  located  near  the  gum  margin  it  may  follow  the 
pericemental  tract  just  as  an  apical  abscess  may  do  and  discharge  at 
the  free  margin.     In  this  case  the  condition  simulates  a  pyorrhoea 

pocket. 

If  the  abscess  begin  near  the  apex  it  may  find  vent  through  the 
gum  and  thus  produce  a  fistula  simulating  that  of  apical  abscess 

(Fig.  536). 

Morbid  Anatomy.  Aside  from  the  state  of  the  teeth  which  show 
evidences  of  a  tendency  to  secondary  dentine  and  nodule  formation, 
it  has  been  noted  that  the  abscess  is  intrapericemental,  not  sub- 

FiG.  535. 


Two  ^-iews  of  an  intrapericemental  abscess.     Pulp  \'ital.     (Kirk.) 

pericemental.  Figs.  535  and  536  show  the  inflammatory  swelling  of 
the  pericementum,  the  central  abscess  cavity,  and  the  loss  by  resorp- 
tion of  the  alveolar  process  may  easily  be  calculated.  The  original 
chronic  nature  of  the  local  irritation  in  this  case  is  evidenced  by  the 
presence  of  hypercementosis. 

In  several  of  these  cases,  where  the  fistulse  have  been  of  long  stand- 
ing, the  editor  has  removed  calculi  (Fig.  537). 

Symptoms.  These  have  been  largely  foreshadowed  in  the  discussion 
of  the  pathology.  Upon  some  vital  tooth  there  appears  an  uneasiness, 
at  first  not  very  painful,  followed  later  by  an  inflammatory  swelling 
which  may  produce  acute  pain  and  then  discharge  a  glairy  fluid  or 


PERICEMENTAL  ABSCESS. 


585 


purulent  matter.  There  is  an  absence  of  the  phlegmonous  inflam- 
matory involvement  of  contiguous  tissues  common  in  cases  of  acute 
apical  abscess.  The  fistula  may  persist  after  the  discharge  and  the 
case  may  first  be  seen  in  this  condition. 

D.  D.  Smith  calls  attention  to  the  absence  of  marked  pain  upon 
tapping,  and  the  production  of  a  feeling  of  apprehension  upon  the 
part  of  the  patient  during  the  stages  preceding  the  formation  of  the 
fistula. 

In  other  cases  the  shifting  of  the  tooth  from  its  position  is  the  first 
noticeable  symptom,  followed  later  by  the  pain,  and  later  still  by  the 
discovery  of  a  pocket  alongside  the  tooth. 


Fig.  536, 


Transverse  section  through  buccal  roots  and  pericemental  abscess  shown  in  Fig.  535,  showing 
intrapericemental  abscess  cavity  with  fistulous  outlet  and  nearby  areas  of  nodular  hypercemen- 
tosis.     (Kirk.) 

In  other  forms  of  gout  urates  exist  in  excess  in  the  urine  after  anti- 
gout  therapeusis  is  applied.  The  inference  is  that  the  local  conditions 
are  relieved  by  the  solution  of  the  urates  in  the  focus  of  inflammation 
and  by  a  general  elimination  of  the  excess  from  the  blood.  They 
re-enter  the  blood  by  way  of  the  lymph  stream  and  are  eliminated 
by  the  kidneys. 

While  the  pericemental  irritation  may  involve  many  teeth,  acute 
outbreaks  are  usually  confined  to  but  one  or  at  most  two  teeth.    The 


586  PERICEMENTAL  ABSCESS. 

disease  subsequently  attacks  other  teeth  singly,  although  these  may 
escape  involvement  for  years. 

It  is  but  just  to  state  that  by  some  prominent  practitioners  the  gouty 
symptoms  are  held  to  be  due  to  a  toxsemia  primarily  originating  in 
the  mouth — i.  e.,  either  mouth  toxins  are  formed  from  oral  detritus 
by  bacteria,  which  toxins  enter  the  alimentary  tract  and  are  absorbed, 
or  the  bacteria  enter  the  intestines  and  there  form  toxins  which  are 
absorbed. 

It  is  held  that  these  toxins  are  responsible  for  kidney  disease  and 
evidences  of  general  malnutrition. 

Before  either  of  the  explanations  offered  can  be  finally  accepted, 
more  corroborative  evidence  of  the  cure  or  failure  of  cure  of  systemic 
conditions  by  oral  prophylaxis,  as  practised  by  D.  D.  Smith,  must 
be  forthcoming.  It  is  to  be  hoped  that  such  cures  are  to  be  so  effected, 
as  it  will  reduce  the  treatment  of  obscure  conditions  to  a  simplicity. 

Diagnosis.  In  making  the  diagnosis  the  symptoms  described  are 
to  be  borne  in  mind,  but  the  disease  may  be  confounded  with  several 
diseases  having  somewhat  similar  symptoms.  An  acute  apical  abscess 
due  to  gangrenous  pulp  may  be  differentiated  by  obtaining  evidences 
of  pulp  death,  previous  root-canal  treatment,  etc.  There  is  also  much 
greater  pain  upon  percussion  than  in  pericemental  abscess. 

If  the  apical  abscess  be  in  the  third  stage  it  may  be  differentiated 
if  any  doubt  exist,  by  incision  and  subsequent  exploration. 

An  acute  lateral  abscess  due  to  a  root  perforation  is  more  difficult 
of  differential  diagnosis,  but  after  incision  evidences  of  perforation 
may  be  sought  externally,  or  the  root  canal  may  be  opened.  In  these 
acute  conditions  the  a;-ray  may  render  valuable  aid.  (See  Fig.  449.) 
The  pulp  being  found  alive  by  any  reliable  test  is  evidence  that  the 
case  is  either  one  of  pericemental  abscess  or  of  acute  traumatic  peri- 
cementitis. In  a  few  cases  of  partial  gangrene  of  the  pulp  the  pulp 
may  test  as  vital,  yet  really  the  symptoms  be  due  to  apical  abscess. 

Acute  traumatic  pericementitis  usually  has  a  history  of  traumatism 
and  presents  more  pain  upon  tapping. 

A  form  of  pericemental  abscess  is  sometimes  found  existing  as  a 
secondary  process  dependent  upon  a  primary  pyorrhoea  of  the  first 
class.  The  pus  burrows  from  the  gum  pocket  into  the  gum  tissue  and 
excites  an  abscess  which  discharges  upon  the  lateral  aspect  of  the  gum. 
The  connection  of  the  sinus  at  the  gum  margin  with  the  fistula  will 
demonstrate  their  relation.     (Figs.  500  and  501.) 

Again,   a  pericemental  abscess  may  be  caused  by  metastasis  of 


PERICEMENTAL  ABSCESS. 


587 


Fig.  537. 


pyogenic  organisms  from  an  acute  apical  abscess — e.  g.,  an  abscess 
in  the  bifurcation  of  the  roots  of  a  molar  may  have  been  caused  by 
bacteria  from  an  apical  abscess;  the  presumption  is  that  the  bacteria 
have  followed  the  pericemental  tracts  perhaps  via  the  glands  of  Black 
or  by  way  of  the  bloodvessels,  and,  finding  a  suitable  location  in  the 
bifurcation,  have  there  developed.  Of  course,  in  such  a  case  the  pulp 
of  the  tooth  in  question,  or  of  that  in  an  adjoining  tooth,  will  be  dead. 
Failing  a  positive  differential  diagnosis,  the  case  should  be  treated 
upon  general  principles — i.  e.,  counterirritation,  derivation,  etc.,  and 
decisive  developments  awaited. 

Prognosis.  The  prognosis  of  the  disease  depends  largely  upon  the 
form  in  which  it  first  exhibits  itself,  and  also  upon  the  length  of  time 
an  increased  amount  of  waste  products  has  been  present  in  the  circu- 
lation. In  all  grades  of  the  inflammation, 
except  that  attended  by  pus  formation,  the 
cure  of  the  general  condition  is  usually  fol- 
lowed by  a  more  or  less  prompt  subsidence  of 
the  dental  symptoms;  although  if  a  tooth  be 
loose  the  condition  may  improve,  but  does  not 
disappear.  If  pus  form,  as  indicated  by  the 
unusual  activity  of  the  inflammatory  symp- 
toms, destruction  of  tissue,  pericemental  and 
alveolar,  it  will  progress  until  it  is  given  vent, 
no  matter  how  active  or  effective  in  other 
particulars  therapeusis  may  be.  In  these  cases  the  tooth  is  usually 
lost  sooner  or  later. 

One  or  more  teeth  may  be  repeatedly  attacked,  and  if  the  underlying 
cause  be  promptly  removed  they  may  partially  recover. 

Treatment,  If  the  pericemental  abscess  discharge  by  way  of  the 
gum  margin,  infection  from  the  oral  cavity  occurs  and  the  pocket 
originally  formed  becomes  deeper.  The  case  simulates  then  a  pyorrhoea 
alveolaris  beginning  at  the  gum  margin.  The  treatment  is  then  con- 
ducted accordingly.  If  the  swelling  occur  upon  the  gum,  at  a  point 
more  or  less  midway  upon  the  root,  it  should  be  opened  under  anti- 
septic precautions.  An  injection  of  cocaine  solution  should  be  made 
and  a  semicircular  flap  raised.  The  diseased  area  should  be  explored 
for  calculus  and,  whether  found  or  not  found,  the  necrotic  tissue  should 
be  curetted  away.  Next  the  pocket  should  be  syringed  out  ^dth 
mercuric  chloride  in  hydrogen  dioxide  1:  1000  or  meditrina.  The  flap 
is  next  stitched  into  place  and  the  gum  painted  over  with  steresol.    (See 


-1,  calculus. 


588  PERICEMENTAL  ABSCESS. 

p.  245.)  The  mouth  should  be  kept  in  an  aseptic  condition  during  the 
liealing  of  the  parts.  Whether  the  exciting  cause  of  this  condition  shall 
be  finally  shown  to  be  bacterial  or  not,  the  predisposing  cause  in  a 
general  malnutrition  or  intestinal  toxaemia  should  be  sought  for  and, 
if  possible,  corrected. 

In  the  elimination  of  the  waste  products  which  act  as  irritants  the 
best  results  seem  to  be  attained  by  measures  directed  to  an  increase 
of  the  general  eliminative  functions,  the  increase  of  tissue  oxidation, 
and  a  restriction  of  diet.  Such  measures  in  general  cause  the  elimina- 
tion of  existing  waste  products  from  the  circulation  and  prevents  the 
formation  of  an  excess  of  new  waste  products. 

The  waste  products  in  the  system  are  dissolved  by  the  copious 
ingestion  of  water.  At  the  same  time  the  blood  pressure  is  raised  and 
the  kidneys  stimulated  to  increased  action  (diuresis).  A  pure  water 
is  of  as  much  value  in  gout  as  one  containing  lithium  salts.^  The 
amount  consumed  daily  should  be  from  five  to  eight  pints,  preferably 
to  be  taken  between  meals;  as  water  taken  at  meals  is  apt  to  interfere 
with  digestion.  It  may  be  necessary  at  times  to  prescribe  salts  of 
lithium  with  the  water  for  the  effect  upon  the  mind  of  the  patient  who 
may  have  an  aversion  to  w^ater.  E.  C.  Kirk  has  recommended  the 
bitartrate  of  lithium,  to  be  administered  in  5-grain  doses,  three  times 
daily  in  water.  Talbot  prefers  thialion,  a  laxative  salt  of  lithium. 
The  use  of  Turkish  or  Russian  baths,  if  not  specifically  contraindicated 
by  acute  or  chronic  disease,  followed  by  massage  of  the  liver  and 
kidneys,  is  valuable  for  the  stimulative  effects  upon  these  organs  and 
upon  the  skin.  During  the  perspiration  induced  by  the  bath  many 
impurities  are  eliminated  from  the  blood. 

If  constipation  exist  the  bowels  should  be  kept  open  by  the  use  of 
laxatives.    It  tends  to  the  production  of  an  intestinal  toxaemia. 

Vigorous  exercise  in  the  open  air,  if  not  contraindicated  by  some 
organic  disease,  is  valuable,  as  it  increases  the  function  of  the  ehmi- 
nating  organs  and  supplies  to  the  tissues  an  abundance  of  oxygen  for 
metabolism.  All  overwork,  worry,  loss  of  sleep,  or  other  causes  tend- 
ing to  neurasthenia  should  be  carefully  avoided.  Anaemia  should  be 
corrected  if  possible,  as  it  signifies  a  lessened  oxidation.  Disorders 
of  the  intestinal  tract  and  its  appendages,  particularly  hepatic  disorders, 
also  demand  correction. 

The  diet  should  be  of  a  character  which  will  lessen  the  formation  of 
urates.    The  amount  of  vegetable  food,  in  proportion  to  animal,  should 

'  Hare,  Practical  Therapeutics. 


PERICEMENTAL  ABSCESS.  589 

be  increased,  thus  raising  the  alkaHnity  of  the  body  fluids.  Red  meats, 
and  white  meats  difficult  of  digestion,  increase  the  formation  of  urates. 
Poultry  and  shell-fish  in  the  dietary  lessen  their  formation.  The 
consumption  of  malt  liquors  notably  increases  it,  and  sweet  wines, 
particularly  champagnes  (both  sweet  and  dry),  are  poisonous  to  gouty 
patients.  Spirituous  liquors  are  also  harmful,  since  they  lessen  tissue 
oxidation  and  produce  gastric  and  hepatic  disturbances  which  cause 
faulty  metabolism. 

Recognizing  the  predisposition  which  exists  in  gouty  persons  to 
active  pericemental  degenerations,  the  operator  should  guard  against 
injuries  to  the  pericementum,  which  might  induce  a  weak  articulation 
and  precipitate  gouty  pericementitis.  Such  teeth  should  not  be 
violently  wedged;  injury  to  the  gum  or  gum  margins,  by  the  use  of 
improper  rubber-dam  clamps,  ligatures  driven  beneath  margins,  etc., 
may  excite  the  first  stages  of  a  degeneration  which  will  end  only  in  the 
loss  of  the  abused  tooth. 


CHAPTER    XXVII. 
REFLEX  DISORDEES  OF  DENTAL  ORIGIN. 

Recognizing  pain  as  a  condition  produced  through  the  overexcita- 
tion of  sensory  nerves,  a  reflex  pain  may  be  defined  as  a  pain  referred  to 
some  point  other  than  that  of  its  origin.  Pain  referred  to  the  distribu- 
tion of  a  sensory  nerve  may  be  due  to  overexcitation  of  any  portion  of 
the  nerve  in  its  terminal  distribution,  to  diseases  affecting  any  portion 
of  the  nerve  trunk,  or  to  disorders  affecting  the  central  termination  of 
the  nerve.  Again,  irritation  of  one  sensory  nerve  may  be  referred  to 
some  other  sensory  nerve.    The  condition  is  called  neuralgia. 

As  both  the  upper  and  the  lower  teeth  and  their  surroundings 
receive  their  neural  supply  from  branches  of  the  fifth  pair  of  cranial 
nerves,  discussion  of  this  subject  is  confined  to  causes  operating  within 
the  distribution  of  that  nerve. 

As  such  general  conditions  as  malaria,  sj'philis,  and  forms  of  anaemia 
operate  to  produce  neuralgia  which  may  be  referred  to  the  teeth,  or  the 
parts  about  them,  only  those  cases  will  be  regarded  as  dental  which 
have  undoubtedly  a  dental  origin,  as  evidenced  by  disappearance  of 
the  neuralgia  following  cure  of  the  exciting  dental  condition.  It  should 
be  noted,  however,  that  vague  and  sometimes  severe  pains  referred 
to  the  teeth  may  entirely  disappear  after  the  cure  of  some  constitu- 
tional disorder.  For  example,  cases  of  periodically  recurring  dental 
pain  have  been  entirely  relieved  through  the  administration  of  quinine 
and  arsenic;  the  pains  were  clearly  of  malarial  origin.  Pain  about  the 
teeth  in  syphilitics  has  disappeared  after  the  administration  of  iodides. 
Pain  referred  to  the  teeth  in  anaemic  patients  has  disappeared  after  a 
long  course  of  chalybeates. 

Reflexes  of  dental  origin  are  both  motor  and  sensory,  the  latter  far 
outweighing  the  former  in  importance.  ]Motor  reflexes  may  be  noted  in 
the  quick  spurt  of  saliva  from  the  ducts  of  the  salivary  glands  upon 
infliction  of  pain  in  the  teeth,  and  by  the  spasmodic  contraction  of  the 
muscles  about  the  mouth  when  the  pulp  of  a  tooth  is  deliberately 
irritated.  Twitching  of  the  muscles  about  the  face  is  a  common 
accompaniment  of  trigeminal  neuralgia. 


Fig.  538. — Plan  of  the  fifth  cranial  nerve,  showing  the  relationships  of  the  dental  ner\-es. 

(After  Flower.) 


592  REFLEX  DISORDERS  OF  DENTAL  ORIGIN. 

Before  direct  association  of  dental  diseases  with  pains  in  other  parts 
can  be  clearly  demonstrated,  a  re^^ew  of  those  conditions  of  the  teeth 
attended  by  pain  must  be  made. 

Dental  pain  arises  in  consequence  of  disorder  of  the  sensory  struct- 
ures; these  are  situated  in  the  pulp,  and  are  continuous  throughout 
the  dentine  and  in  the  pericementum.  The  roots  of  teeth  may  have 
unusual  anatomical  relations  with  other  sensory  structures  than  their 
own  pericementum.  Dental  pains,  therefore,  may  be  discussed,  first, 
in  connection  with  affections  of  the  dentine  and  pulp  and,  secondly, 
with  those  of  the  pericementum. 

It  was  stated,  in  discussing  the  diseases  of  the  dental  pulp,  that  this 
organ  is  not  the  seat  of  the  tactile  sense  and  that,  like  other  organs 
ha\dng  a  kindred  physiological  relationship,  irritation  excited  in  it  is 
not  located,  but  is  referred  to  some  other  part.  While  all  reflex  dental 
disturbances  are,  as  a  rule,  located  in  some  part  of  the  great  nerve 
branch  supplying  the  source  of  irritation,  the  irritation  may  be  reflected 
to  distant  parts :  first,  of  the  same  cranial  nerve,  and,  secondly,  to  other 
nerves.  That  is,  pain  having  its  origin  in  one  of  the  upper  teeth  is 
most  likely  to  be  referred  to  a  point  or  points  in  the  distribution  of  the 
superior  maxillary  nerve.  Disturbances  in  or  about  the  lower  teeth  are 
usually  referred  to  the  distribution  of  the  inferior  maxillary  nerve.  In 
affections  of  either  upper  or  lower  teeth  the  pain  may  be  referred  to  the 
first  division  of  the  fifth  nerve.  In  all  of  these  cases,  but  most  notably 
in  connection  with  disturbances  of  the  upper  teeth,  the  usual  symptom 
of  trifacial  neuralgia — tenderness  of  the  supra-orbital  and  infra-orbital 
nerves  at  their  points  of  emergence  upon  the  face,  the  supra-orbital 
and  infra-orbital  foramina — is  commonly  present. 

Cases  are  extremely  rare  where  the  reflex  pain  is  referred  to  the 
opposite  side;  indeed,  so  unusual  is  this  occurrence  that  its  mention 
warrants  suspicion  that  other  sources  of  irritation  exist  upon  the  side 
referred  to. 

The  extent  of  acuteness  of  reflex  pain  bears  no  direct  relation  to  the 
apparent  extent  of  the  source  of  irritation. 

As  might  be  surmised  from  the  function  of  the  dental  pulp,  painful 
reflex  dental  disorders  are  more  common  in  connection  with  diseases 
of  the  pulp  than  with  those  of  the  pericementum. 

REFLEX  NEURALGIA  FROM  EXPOSED  DENTINE. 

The  exposure  of  the  dentine  to  external  sources  of  irritation  is 
followed  by  reactions  governed,   first,   by  the  degree  of  sensitivity 


REFLEX  NEURALGIA  FROM  EXPOSED  DENTINE.  593 

inherent  in  the  protoplasm  of  the  tissue;  and,  secondly,  by  the  degree 
of  hypersensitivity  induced  in  it.  Reflex  disturbance  due  to  these 
irritations  is  more  common  in  the  class  of  persons  called  "neuralgics" 
than  in  other  persons.  Like  direct  pulp  pains,  unless  actual  pressure 
be  exerted  upon  the  affected  tissue,  there  is  no  localized  pain.  In  the 
absence  of  deliberate  irritation,  the  pain  may  be  referred  to  any  portion 
of  the  peripheral  distribution  of  the  fifth  nerve  upon  the  face;  but  if 
an  acid  liquid  such  as  lemon-juice  or  vinegar,  or  sugars,  be  taken  into 
the  mouth,  pain  is  excited,  which  is  referred  indefinitely  to  the  teeth  of 
one  side,  frequently  of  one  jaw.  Reflex  pains  due  to  this  cause  are 
much  more  likely  to  appear  when  there  is  but  little  loss  of  dentine. 

When  carious  cavities  have  proceeded  to  any  depth  evidences  of 
direct  pulp  disturbance  are  obtained  through  the  increased  response 
to  thermal  changes. 
X  Reflex  pains  from  exposed  dentine  appear  most  common  in  con- 
nection with  exposures  at  the  neck  of  the  tooth  and  upon  abraded 
areas.  Obstinate  and  persistent 
neuralgia,    positively    referred    to 

another  nerve  branch,  may  appar-  |^^       ^-^^a..^^<*rs 

ently  owe  its  origin  to  so  slight  a  • — ^PT^  |  iMM^.%M 

cause  as  exposure  at  the  neck  of  a      /^^^        I  .^B     ftHwrni 
tooth  of  a  line  of  dentine  (Fig.  539).     \%jlf  \%m  m,  m 

The  proof  of  the  connection  be-       ^^  ^^1*^^%*.^ 

tween  the  two  is  made  clear  by  a     ^^''°^  '^"'^f  ?  "^^T  ^'•^'^.^^^^^^  ^^^°''^- 

•/  ated  with  reflex  pams. 

disappearance  of  the  neuralgia  after 

the  exposed  dentine  has  been  subjected  to  the  action  of  powerful 
caustics,  destroying  the  dentinal  filaments  to  some  depth.  The  con- 
nection between  the  two  may  be  revealed  only  by  accident;  the 
contact  of  a  toothpick,  a  dental  instrument,  or  the  finger-nail  may 
induce  a  paroxysm  of  pain. 

While  in  some  cases  the  dental  origin  of  reflex  pain  may  be  made 
clear  by  the  induction  of  a  painful  response  in  the  area  of  reflection, 
by  irritating  a  tooth  pulp,  this  reaction  is  not  constant.  The  causal 
relation  is  only  certain  when  the  cure  of  localized  dental  disease  is 
followed  by  a  disappearance  of  the  neuralgia  without  further  treat- 
ment.   This  proof  should  be  exacted  in  all  cases. 

The  most  common  sources  of  neuralgic  attacks  about  the  face  are 
diseases  of  the  eyes  and  teeth.  In  general  terms,  diseases  of  the  eye 
give  rise  to  reflex  pains  referred  to  the  distribution  of  the  first  branch 
of  the  fifth  nerve;  diseases  of  the  teeth  usually  cause  reflex  pains  in 

38 


594  REFLEX  DISORDERS  OF  DEXTAL  ORIGIN. 

either  the  superior  or  inferior  maxillary  divisions,  according  as  the 
upper  or  lower  teeth  are  affected.  In  all  painful  affections  of  these 
nerves  attention  should  at  once  be  directed  to  the  organs  named. 


REFLEX  NEURALGIAS  FROM  PULP  DISEASES. 

The  disturbances  require  classification  according  to  the  distance 
between  their  source  and  their  manifestations. 

In  the  Fifth  Pair  of  Nerves.  Pain  referred  to  a  different  spot 
or  area  than  its  origin  is  a  characteristic  of  all  pulp-diseases.  The 
extent  of  its  reflection  depends,  first,  upon  the  patient,  as  noted  in  con- 
nection wdth  the  reflex  pains  from  exposed  dentine;  and,  secondly,  upon 
the  variety  of  pulp  disease.  In  neuralgic  patients  any  variety  of  pulp 
disease  may  cause  comparatively  distant  pains.  But,  as  Black  has 
pointed  out,^  the  general  rule  is,  that  the  more  chronic  and  profound 
degenerative  diseases  of  the  pulp  are  much  more  hable  to  give  rise  to 
distant  reflex  pains  than  are  acute  pulp  diseases. 

The  pains  of  acute  hypersemia  and  of  acute  inflammation  of  the 
pulp  are  usually  referred  to  the  region  of  the  tooth  affected,  or  to  a 
corresponding  nerve  trunk.  In  conditions  of  venous  hypersemia^ 
nodular  calcifications,  chronic  inflammation,  and,  later,  pulp  degen- 
erations, the  pains  may  be  of  such  character  that  their  dental  origin 
is  only  determined  after  persistent  search.  Particularly  is  this  true 
of  the  growth  of  pulp  nodules.  The  source  of  the  reflex  pains  is  all 
the  more  obscure  from  the  fact  that  in  these  chronic  degenerations 
direct  dental  symptoms  may  be  entirely  absent,  and  are  only  elicited 
upon  the  most  searching  examination  and  exhaustive  tests. 

There  is  no  constancy  in  the  location  of  the  pain  due  to  any  of 
these  causes;  but  tenderness  of  the  eyeball  upon  pressure;  persistent 
pain  in  the  temporal  and  anterior  auricular  regions,  particularly  in 
connection  with  pulp  diseases  of  the  lower  posterior  teeth;  in  the  ear 
itself,  a  common  site  of  the  reflex  pain  excited  by  chronic  pulp 
inflammation  and  suppuration  of  that  organ;  behind  the  ear,  back  of 
the  lower  border  of  the  mastoid  processes,  tender  spots  may  develop; 
tenderness  to  pressure  may  appear  at  the  supra-orbital  and  infra- 
orbital or  mental  foramen,  and  about  the  chin.  In  the  same  class  of 
diseases  the  pains  may  frequently  radiate  as  far  as  the  shoulder.  Many 
of  these  cases  receive  attention  from  the  general  practitioner,  and  the 
painful  attacks  recurring  at  irregular  intervals  are  relieved  by  analgesic 

1  American  System  of  Dentistry,  vol.  i. 


REFLEX  PAINS  FROM  DISEASES  OF  THE  PERICEMENTUM.     595 


-and  no  attention  paid 
It  should  be  a  routine 


Fig.  540. 


Spots  of  tenderness  in  reflex  neural- 
gias of  dental  origin. 


remedies — phenacetin,  acetanilid,  exalgin,  etc- 
to  a  probable  dental  source  of  the  disorder, 
practice  to  examine  the  teeth  in  cases 
presenting  pains  of  the  type  and  in  the 
situations  described.  Immediate  search 
should  be  made  for  teeth  containing  pulps 
in  late  degenerative  stages.  (See  Symp- 
toms of  Diseases  of  the  Pulp.)  Acute 
diseases  of  the  pulp,  including  suppu- 
ration and,  notably,  abscess  of  the  pulp, 
usually  have  attention  directed  to  the 
teeth  through  pain  induced  by  thermal 
changes,  so  that  their  diagnosis  is  cjuickly 
made.  Not  so,  however,  with  the  chronic 
degenerative  changes,  except  possibly  of 
pulp  nodules;  for  if  the  pulp  is  in  the  late  stages  of  degeneration,  it 
may  require  repeated  applications  of  cold  and  heat  to  elicit  a  response 
from  teeth  which  do  not  respond  by  tenderness  upon  percussion. 

Failing  to  obtain  evidence  of  pulp  disorders,  examination  should 
be  made  for  exposed  and  hypersensitive  dentine.  Then,  examination 
of  the  pericemental  reaction  of  each  tooth  should  be  made,  and  for  any 
evidences  about  the  teeth  pointing  to  pericemental  disturbance.  (See 
later.) 

Lauder  Brunton^  records  that,  in  his  own  case,  temporal  neuralgia 
accompanied  by  tender  eyeball  was  found  due  to  exposed  dentine  upon 
the  posterior  cervical  surface  of  a  lower  third  molar  (Fig.  522).  The 
same  writer^  announces  "that  so  frequently  are  headaches  dependent 
upon  decayed  teeth  that  in  all  cases  of  headache  the  first  thing  I  do 
is  to  carefully  examine  the  teeth;"  as  should  everyone  else.  Brunton 
explains  the  painful  reaction  upon  the  accepted  hypothesis  of  the 
pathology  of  megrim,  that  it  is  due  to  spasmodic  contraction  of  the 
peripheral  end  of  an  artery,  with  dilatation  of  the  proximal  portion. 
"Irritation  in  the  tooth  is  reflected  to  the  cervical  sympathetic  ganglia 
and  causes  spasmodic  contraction  of  the  arteries  through  irregular 
stimulation  of  the  vasomotor  nerves." 


REFLEX  PAINS  FROM  DISEASES  OF  THE  PERICEMENTUM. 

As  a  general  rule,  pericemental  pains  are  located  at  the  affected 
tooth;  but  in  some  of  the  disorders,  particularly  those  in  which  eitlier 


1  St.  Bartholomew's  Hosp.  Rep.,  vol.  xix.     Eeprinted  in  his  Disorders  of  Digestion.         -  Ibid. 


596  REFLEX  DISORDERS  OF  DENTAL  ORIGIN. 

hypernemia  or  inflammation,  acute  or  chronic,  is  not  present,  the 
teeth  may  not  be  tender  upon  percussion,  and  yet  excite  reflex  pains 
in  other  parts,  the  proof  of  the  connection  being  determined  by  a  dis- 
appearance of  the  pain  upon  extraction  of  the  tooth.  The  roots  in 
such  cases  usually  present  either  an  hypertrophy  of  cementum  or  show- 
that  resorption  of  a  portion — it  may  be  a  major  portion — of  the  root 
has  occurred. 

In  cases  of  hypercementosis  it  is  assumed  that  the  source  of  the 
irritation  is  pressure  upon  the  nerves  of  the  pericementum  by  the 
hypertrophic  growth.  Very  widespread  disorders  may  arise  from  this 
source. 

Flagg  records^  many  varieties  of  trifacial  neuralgia;  pains  in  remote 
parts  of  the  body;  grave  functional  disorders  of  the  eye  and  ear;  and 
motor  disturbances — chorea,  epilepsy,  and  paralysis — having  a  direct 
demonstrable  connection  with  hypercementosis.  Insanity  has  also 
been  produced. 

He  mentions  violent  attacks  of  trifacial  neuralgia  as  the  most  com- 
mon reflex  disturbance  from  this  source;  and  next,  long-continued 
pains  in  the  ear  or  eye  of  the  affected  side.  The  existence  of  acute 
disease  of  these  organs  is  usually  diagnosed  by  the  general  prac- 
titioner. He  states  that  oral  and  ocular  disturbances,  both  functional 
and  painful,  are  of  gradually  increasing  severity. 

In  examining  for  a  dental  source  of  such  pains,  exposed  dentine, 
pulp  diseases,  and  inflammatory  affections  of  the  pericementum  should 
be  first  excluded.  In  examinations  by  percussion  a  different  response 
may  be  obtained  from  some  one  tooth  than  from  the  others.  Hyper- 
cementosis of  a  particular  tooth  is  indicated  by  finding  the  gum  line 
slightly  receded  and  the  tooth  attachment  unusually  firm;  if,  in  addi- 
tion, vague,  heavy,  dental  pains  have  persisted  at  intervals  over  a  long 
period,  the  diagnosis  is  probable.  It  is  only  certain  w^hen  tapping 
upon  the  tooth  brings  on  a  paroxysm  of  neuralgia,  or  w'here  a  skia- 
graphic  view  actually  exhibits  the  hypertrophic  growth.  The  remedy 
is  extraction.  Any  root  fragment  left  unextracted  may  perpetuate  the 
reflex  disorder. 

Painful  affections  referred  to  the  neighboring  region  of  the  affected 
tooth,  or  diffused  through  the  distribution  of  the  corresponding  nerve 
trunk,  or  to  the  eye  or  ear,  may  accompany  the  process  of  resorption 
of  the  roots  of  permanent  teeth.  Gillman^  records  a  case  where  facial 
paralysis  disappeared  upon  extraction  of  a  tooth  which  had  long  been 

1  Dental  Cosmos,  1878.  ^  Boston  Medical  and  Surgical  Journal,  1867. 


IMPACTED  TEETH  AS  A  CAUSE  OF  NEURALGIA.  597 

the  seat  of  disturbance  and  which,  upon  extraction,  revealed  resorp- 
tion of  its  root.  In  these  obscure  cases  the  skiagraph  if  taken  at  once 
will  be  a  great  aid  in  the  exclusion  or  diagnosis  of  pericemental  and 
root  abnormalities. 

All  of  the  acute  or  chronic,  septic  or  non-septic,  inflammations  of  the 
pericementum  may  give  rise  to  reflex  pains.  In  many  of  these  cases 
the  cause  of  the  reflex  irritation  is  due,  perhaps,  to  sepsis,  rather  than 
to  a  pure  neurotic  connection.  The  most  common  causes  of  the  reflex 
pains  are  found  in  that  stage  of  pericemental  irritation  which  antedates 
acute  septic  apical  pericementitis,  and  which  accompanies  the  chronic 
inflammations  of  the  apical  pericementum  from  any  cause.  In  some 
of  these  cases  reflex  neuralgia  may  play  a  subordinate  part  to  general 
infection  from  the  focus  of  disease.  The  reflex  nervous  disorders  con- 
sist in  painful  disturbances  in  the  distribution  of  the  fifth  nerve  and 
disorders  of  special  senses,  particularly  that  of  hearing.  Unless  an 
exacerbation  of  the  reflex  disorder,  or  symptoms  referable  to  that 
region,  be  induced  by  pressure  or  percussion  on  the  tooth,  a  causal 
relationship  is  only  made  out  by  either  relieving  an  existing  dental 
disorder,  an  x-ray  skiagraph,  or  extracting  the  teeth.  The  symptoms 
of  septic  intoxication  and  septicsemia  must  be  carefully  differentiated 
from  reflex  neuralgias  in  such  cases:  the  latter  are  rare;  the  former 
probably  more  frequent  than  supposed  in  connection  with  septic 
dental  diseases. 

IMPACTED  TEETH  AS  A  CAUSE  OF  NEURALGIA. 

Neuralgia  of  varying  degrees  of  severity  is  a  common  accompaniment 
of  impacted  teeth.  It  is  most  frequently  noted  in  connection  with  erup- 
tion of  the  lower  third  molars,  not  only  because  this  tooth  is  the  one 
most  frequently  impacted,  but  because  of  the  anatomical  relations  of 
its  roots  with  the  inferior  dental  nerve. 

In  the  milder  forms  of  impaction,  those  in  which  eruption,  though 
delayed,  is  subsequently  completed,  the  pains  are  commonly  localized 
and  associated  with  but  occasional  attacks  of  rigidity  of  the  masseter 
muscles.  If,.however,  the  crown  present  horizontally  or  nearly  so,  and 
its  progress  is  arrested  by  impaction  against  the  posterior  wall  of  the 
lower  molar,  or  if  its  progress  be  arrested  by  permanent  imprisonment 
of  the  advancing  crown  between  the  posterior  surface  of  the  second 
molar  and  the  base  of  the  coronoid  process,  not  only  may  intense  local 
pains  be  induced,  but  severe  reflex  disturbances  of  both  a  sensory  and 
motor  character  may  occur.    In  some  of  these  cases  root  formation  is 


598  REFLEX  DISORDERS  OF  DENTAL  ORIGIN. 

completed,  although  the  crown  of  the  tooth  does  not  advance,  in  which 
case  compression  of  the  inferior  dental  canal  and  its  contents  may 
occur  and  cause  grave  reflex  disturbances.  The  local  irritation  about 
the  root,  due  to  root  growth,  may  excite  continued  constructive  action 
by  the  pericementum,  and  the  hypertrophic  growth  in  its  turn  may 
be  the  source  of  reflex  neuralgias. 

Complete  imprisonment  of  the  entire  tooth  has  been  found  to  be  the 
exciting  cause  of  facial  neuralgias,  for  the  cure  of  which  extensive 
surgical  operations  have  been  performed. 

Impacted  cuspids  and  other  teeth  may  excite  no  other  symptoms 
than  reflex  neuralgia.  The  possible  connection  between  an  impacted 
tooth  and  neuralgia  is  made  out  after  excluding  other  dental  causes, 
when  it  may  be  observed  that  one  or  more  of  the  permanent  teeth  are 
absent  from  the  dental  arch,  at  dates  long  after  their  normal  time  of 
eruption. 

A  condition  equivalent  to  partial  impaction,  in  which  dental  irrita- 
tion may  be  the  source  of  reflex  neuralgia,  is  seen  when  the  teeth  are 
crowded — jammed  into  arches  too  small  for  their  accommodation. 
During  the  period  of  eruption  severe  maxillary  pains  may  recur  at 
intervals. 

PAIN  REFERRED  TO  NERVOUS  TRACTS  OTHER  THAN  THE  FIFTH. 

The  most  common  disturbance  appearing  in  other  cerebrospinal 
nerves  than  the  fifth,  due  to  dental  diseases,  is  an  aftection  of  the 
eighth  or  auditory  nerve.  Cases  of  deafness  have  been  recorded  due 
to  diseases  of  both  pulp  and  pericementum,  notably  to  hypercementosis. 
Deafness  which  has  persisted  for  a  long  period  has  been  markedly 
lessened  by  the  extraction  of  teeth  the  seat  of  disease.  Cases  of  sup- 
purative otitis  media  have  been  regarded  as  having  pathological  asso- 
ciation with  septic  diseases  about  the  teeth,  from  the  fact  that  the  aural 
trouble  subsided  immediately  after  extraction  of  the  diseased  teeth. 

Sensory  disturbances  of  the  eye,  associated  with  dental  diseases,  have 
been  alluded  to;  in  addition  to  these,  grave  structural  and  functional 
diseases  of  the  eye,  traceable  to  dental  causes,  have  been  recorded, 
such  as  motor,  sensory,  and  special  sense  disturbances,  together  with 
trophic  disorders.^  Among  the  latter  may  be  mentioned  corneal 
inflammation  and  ulceration  and  phlyctenular  conjunctivitis.  These 
are  probably  due  in  part  to  reflex  trophic  disturbances. 

1  See  Brubaker,  American  System  of  Dentistry,  vol.  iii.,  for  very  full  and  detailed  discussion  of 
these  subjects. 


MOTOR  DISTURBANCES  FROM  DENTAL  DISEASES.  599 

Irregular  paralyses  of  the  third,  fourth,  and  sixth  nerves  of  the 
affected  side  have  been  noted. 

Amblyopia  and  functional  blindness  without  retinal  conditions  to 
account  for  it  have  been  found  to  arise  from  notably  advanced  degen- 
erative changes  in  the  dental  pulp,  sight  returning  to  the  eye  after 
loss  of  a  diseased  tooth.  De  Witt^  records  a  most  instructive  case 
where  temporary  blindness  was  associated  with  septic  apical  peri- 
cementitis, disappearing  after  evacuation  of  the  abscess  and  reappear- 
ing when  secondary  inflammatory  action  arose  in  the  pericementum. 
The  ocular  affection  disappeared  permanently  and  almost  entirely  with 
the  loss  of  the  tooth.  The  history  of  this  case  illustrates  the  important 
causal  relationship  of  reflex  disturbances  with  late  pulp  degenerations ; 
for  the  blindness  arose  two  months  after  some  teeth  were  filled,  and 
existed  for  twelve  years  before  the  septic  apical  pericementitis  appeared. 

A  careful  examination  of  these  and  all  other  reflex  disturbances 
shows  that  pulp  degenerations  outnumber  all  other  affections  as  causes. 
Many  or  most  of  the  cases  are  recorded  by  general  practitioners,  who 
make  no  distinction  between  diseases  of  the  pulp  and  those  of  the  peri- 
cementum, but  a  reliable  diagnosis  of  the  conditions  is  made  possible 
by  the  accompanying  descriptions. 

Cases  of  ovarian  and  uterine  neuralgia  and  sciatica  and  cases  of 
obstinate  pains  in  the  toes  and  fingers  have  been  traced  to  dental 
irritation  of  some  one  of  the  varieties  named ;  the  proof  of  association 
being  disappearance  of  the  pain  with  loss  of  the  tooth. 

MOTOR  DISTURBANCES  FROM  DENTAL  DISEASES. 

Motor  disturbances  due  to  dental  irritation  may  occur  as  recurrent 
or  persistent  contraction  or  paralysis  of  muscles,  together  with  more  or 
less  general  chorea;  in  rare  instances  epilepsy  and  hystero-epilepsy. 
Twitching  of  muscles  of  the  affected  side  of  the  face,  ranging  from 
slight  affection  of  the  occipitofrontalis  or  orbicularis  palpebrarum 
to  recurring  spasm  of  the  elevators  and  depressors  of  the  lower  lip, 
are  far  from  uncommon  phenomena  attendant  upon  pulp  diseases. 
In  one  case  mentioned  by  Guilford^  a  pulp  nodule  was  the  cause  of 
tic  douloureux  of  two  years'  standing. 

Contraction  of  the  masseter  muscle  is  a  common  accompaniment  of 
retarded  eruption  of  the  lower  third  molar,  which  may  be  intensified 
until  the  condition  is  fitly  termed  trismus,  in  some  cases  of  partial 

'  Quoted  by  Brunton,  Disorders  of  Digestion;  2  Private  communication. 


600  REFLEX  DISORDERS  OF  DENTAL  ORIGIN. 

impaction  of  the  teeth.  Partial  trismus  has  been  found  clue  to  a  general 
overcrowding  of  the  dental  arch.'  Records  of  cases  of  torticollis,  due 
to  dental  diseases,  are  also  given  by  Brubaker. 

Cases  of  facial  paralysis,  and  cases  of  paralysis  of  one  arm,  of  para- 
plegia and  hemiplegia,  and  even  of  general  paralysis,  have  been  noted 
as  disappearing  after  the  extraction  of  diseased  teeth.  It  is  noteworthy 
that  in  these  cases,  as  well  as  in  several  cases  of  tetanus  recorded,  the 
probability  of  an  infection  entered  into  the  pathogenesis  of  the  nervous 
diseases. 

Stellwagen^  records  a  case  where  symptoms  of  partial  hemiplegia 
followed  upon  the  operation  of  capping  the  pulps  of  two  molar 
teeth;  the  symptoms  disappeared  promptly  upon  extraction  of  these 
teeth. 

Cases  of  insanity  arising  from  dental  diseases  have  been  recorded; 
they  were  both  maniacal  and  melancholic.  In  several  of  them  a 
restoration  to  a  normal  mental  state  followed  promptly  upon  removal 
of  the  offending  teeth.  In  some  of  these  cases  a  pre-existing  maxillary 
neuralgia  directed  attention  to  the  teeth  as  possible  sources  of  the 
nervous  diseases. 

DENTAL  PAIN  ARISING  FROM  OTHER  THAN  DENTAL  SOURCES. 

Conditions  of  pain  the  reverse  of  those  discussed — i.  e.,  pain  defi- 
nitely or  indefinitely  located  in  teeth  which  exhibit  no  morbid  con- 
ditions whatever — demand  occasional  attention  at  the  hands  of  the 
dentist. 

Chronic  malarial  poisoning,  as  stated  in  the  beginning  of  this 
chapter,  may  give  rise  to  periodical  attacks  of  maxillary  neuralgia. 
As  in  the  gouty  cases,  the  constitutional  cause  of  the  disturbance  is 
made  clear  through  the  therapeusis  most  effective,  viz.,  the  periodical 
recurrence  of  the  pain  leads  to  the  inference  of  a  malarial  origin,  and 
to  the  administration  of  quinine. 

Syphilitic  pains  in  the  jaws  have  a  pericemental  character,  and  other 
evidences  of  syphilis  are  present  which  point  to  a  diagnosis. 

Pains  in  or  about  the  teeth  are  occasional  accompaniments  of  dis- 
eases of  the  brain  or  its  vessels,  and  of  diseases  of  the  uterus,  kidneys, 
and  bladder. 

Disease  in  any  portion  of  the  fifth  cranial  nerve  may  cause  pain 
referred  to  the  teeth. 

'  Brubaker.  2  Private  communication. 


DENTAL  PAIN  ARISING  FROM  OTHER  THAN  DENTAL  SOURCES.    QQ  [ 

Dental  pain  during  pregnancy,  without  any  direct  evidence  of  dental 
disease,  is  relatively  common. 

Disorders  of  the  lower  bowels,  causing  constipation,  may  give  rise 
to  pain  referred  to  one  or  more  teeth,  the  pain  ceasing  promptly  upon 
the  administration  of  an  active  evacuant. 

Treatment  of  Facial  Neuralgia.  The  cause  should  be  sought  for, 
and,  if  possible,  removed.  If  due  to  diseases  of  the  teeth  these  should 
be  relieved;  if  due  to  eye  disease  this  should  receive  attention.  Should 
one  not  discover  the  cause,  yet  desire  to  afford  a  relief  pending  its 
discovery,  the  accepted  remedies  antipyrin,  acetanilid,  and  phenacetin, 
combined  with  caffeine  or  the  bromides,  are  useful. 

Jfe — Antipyrini  (vel  phenacetini  vel  acetanilidi),  5j. 

Caffeinse  citratis,  gr.  x. 

Potassii  bromidi,  5iij. — M. 

Ft.  in  chart.  No.  x. 
Sig. — One  every  thirty  minutes  until  reUeved.     (Hare.) 

If  the  patient  be  constipated  the  bowel  should  be  freed  of  toxic 
substances  by  the  use  of  castor  oil,  repeated  as  necessary. 

In  obstinate  neuralgia  and  other  painful  affections  with  unremov- 
able cause,  the  application  of  the  ri'-rays  has  been  urged  by  Morton 
as  highly  eflBcacious. 


CHAPTER   XXVIII. 
IXFECTIONS  OF  AND  FROM  THE  MOUTH,  AND  STERILIZATION. 

The  conditions  found  in  the  human  mouth,  as  pointed  out  in 
Chapter  III.,  are  of  a  character  which  afford  lodgement  to,  and 
opportunities  for  multipHcation  of,  many  forms  of  bacteria,  both  sapro- 
phytic and  parasitic.  The  oral  conditions  are,  however,  not  entirely 
constant,  so  that  at  different  periods  they  may  favor  the  develop- 
ment of  some  special  bacterial  forms  more  than  others.  The  nature 
of  these  variations  has  not  been  made  out,  although  their  effects  are 
indubitable.  Again,  the  oral  bacterial  inhabitants  are  not  constant 
as  to  species,  for  while  there  are  many  forms  which  appear  to  be 
invariable  occupants  of  the  oral  cavity,  many  pathogenic  forms  are  but 
accidental  residents.  Becoming  resident,  they  may  or  may  not  develop 
according  as  they  find  in  the  mouth  a  suitable  soil.  The  nature  of  what 
constitutes  a  suitable  or  unsuitable  soil  has  not  been  determined,  though 
in  some  cases  extra-oral  culture  experiments  furnish  some  indications. 

Bacterial  growths,  as  causes  of  dental  caries  and  diseases  of  the 
pulp  and  pericementum,  have  been  discussed  in  connection  with  those 
several  diseases.  It  was  shown  that  the  pyogenic  cocci  are  almost 
constant  inhabitants  of  the  human  mouth.  There  appeared  also 
evidence  that  some  of  the  reflex  disorders  of  distant  parts  are  directly 
traceable  to  septic  processes  about  the  teeth,  and,  in  addition  to  these, 
suppurative  diseases  in  other  parts  become  curable  after  removal  of  a 
septic  tooth;  such  conditions  representing  infection  from  a  local  dental 
infection,  an  important  aspect  of  dental  pathology. 

The  infections  arising  from  the  growth  of  mouth  fungi  are  local  and 
general.  The  phrase  fungi  is  used  in  this  connection,  because  other 
classes  besides  the  fission  fungi  (schizomycetes)  are  pathogenic  also. 
Both  the  thread  fungi  (hyphomycetes)  and  bud  fungi  (blastomycetes) 
may  induce  morbid  conditions  in  the  human  mouth. 

The  notable  fungus  of  the  blastomycetes  is  the  saccharomyces  albi- 
cans; this  organism,  when  classified  by  mycologists  as  a  thread  fungus, 
was  known  as  the  oidium  albicans  (Fig.  541).  The  growth  of  this 
organism  illustrates  forcibly  the  influence  of  soil  on  the  growth  of 


INFECTIONS  OF  AND  FROM  THE  MOUTH. 


603 


fungi.  It  does  not  occur  in  the  mouths  of  heaUhy,  well-nourished, 
and  clean  children  with  good  surroundings.  It  is  a  disease  of  child- 
hood, particularly  of  nurslings,  and  its  occurrence  is  almost  always 
confined  to  bottle-fed  babies  whose  feeding  bottles  are  kept  in  an 
unclean  condition.  Debility  of  the  oral  tissues  is  established  in  con- 
sequence of  the  fermentations  arising  from  the  source  just  named, 


Fig.  541. 


Saccharomyces  albicans,  thrush  fungus. 

(Miller.) 

furnishing  a  favorable  condition  for 
the  development  of  the  saccharomyces 
(oidium)  albicans.  The  condition  pro- 
duced is  known  as  thrush.  The  infec- 
tion may  be  carried  from  one  child  to 
another,  and  if  the  fungus  be  brought 
in  contact  with  an  abraded  mucous 
surface  of  an  adult  it  may  develop. 

The  fungus  burrows  between  the 
epithelial  cells  of  the  mucous  mem- 
brane (Fig.  542),  not  beyond  it.  It 
first  appears  in  small  spots,  which 
coalesce,  until  large  patches  of  a  membranous-like  growth  cover  exten- 
sive surfaces,  spreading  by  continuity  to  all  of  the  mucous  surfaces 
associated  with  the  mouth. 

As  bud  fungi  flourish  only  in  media  of  acid  reaction,  the  use  of 
alkaline  washes  is  indicated  in  the  treatment  of  this  condition.  Wiping 
the  patches  with  dilute  phenol-sodique  is  efficacious.  Small  spots 
may  be  cauterized. 

The  hyphomycetes,  or  thread  fungi,  although  associated  with  dis- 
eases of  the  human  skin,  have  not  had  any  pathological  significance 
attached  to  them  as  regards  the  niouth. 


Pavement  epithelium  covered  with 
spores  of  the  oidium  albicans.  (Ch. 
Robin.) 


604  IXFECTIOXS  OF  AXD  FROM  THE  MOUTH. 

INFECTIVE   BACTERIA  OF  THE  MOUTH. 

Bacteria,  being  ever  present,  must  always  play  a  part  in  either 
originating,  modifying,  or  associating  with  all  oral  diseases. 

That  the  progressive  decomposition  of  albuminous  substances, 
always  present  in  the  mouth  to  a  greater  or  less  degree,  by  the  action 
of  saprophytic  fungi,  must  give  rise  to  derivatives  of  albumin,  many 
of  them  toxic  in  effect,  would  be  surmised  even  in  the  absence  of 
experimental  demonstration,  a  suspicion  confirmed  by  experiment. 
Vulpian^  produced  septicaemia  by  vaccinating  animals  with  the  saliva 
of  a  healthy  man.  Griffin^  showed  that  the  parotid  saliva  (pure)  is 
harmless.  The  saliva,  if  boiled,  exerts  no  toxic  action,  from  which 
it  is  clear  that  it  derives  its  toxic  substances  from  the  mouth.  The 
saliva  of  individuals  differs  at  times  in  the  degree  of  its  poisonous 
action.    In  some  diseases  it  becomes  intensely  toxic. 

Of  the  many  oral  bacterial  forms,  some  are  cultivable  and  some 
are  not;  hence  the  specific  effects  of  some  are  discovered,  others  are 
doubtful. 

With  regard  to  local  affections,  other  than  those  described  in  the 
body  of  this  book,  a  bacterial  causation  has  been  made  out  in  some, 
but  in  others  it  has  not. 

STOMATITIS. 

Definition.  By  stomatitis  is  meant  a  catarrhal  inflammation  of  the 
mucous  membrane  of  the  mouth. 

Varieties.  It  may  be  localized,  as  in  marginal  gingivitis,  or  be 
diffuse;  and,  again,  be  accompanied  by  localized  tissue  destructions — 
ulcerations;  the  character  of  the  ulceration  differs  according  to  its 
probable  causes. 

Occurrence.  ]Most  of  these  diseases  belong  to  the  period  of  child- 
hood, although  localized  ulcerative  stomatitis  may  appear  in  the 
aduh. 

Causes.  The  causes  of  stomatitis  are  so  many  and  varied  as  to 
suggest  a  classification  under  heads  according  to  assignable  causes. 
While  it  is  true  that  bacterial  infection  has  not  been  shown  to  be  a 
direct  cause  of  all  of  these  conditions,  some  degree  of  causal  relation- 
ship is  probable  in  all  of  them.  The  disease  may,  however,  be  included 
under  two  heads  according  as  they  are  or  are  not  localized,  and  necrotic. 
The  less  localized  cases  appear  as  a  diffuse  catarrhal  affection,  affect- 

1  Quoted  by  Miller.  2  j\)[d. 


STOMATITIS. 


005 


ing  wide  areas  of  the  oral  mucous  membrane;  the  others  appear  as 
spots  of  locaHzed  tissue  destruction  attended  by  surrounding  h}^er- 
semia. 


Catarrhal  stomatitis 


Local 


f  Simple. 
^  Infectious 


Eruptive  fevers. 
Syphilis. 
Tuberculosis. 
I  Symptomatic  ^  Typhoid  fever. 


Drug  action  . 


Ulcerative  stomatitis . 


r  Local 


L  Symptomatic 


Aphthae. 

Thrush. 

Noma. 
I   Herpes. 
[  Syphilis  (primary). 


(  Fermentations. 
'i  Diphtheria. 
Gonorrhoea. 


f  Iodides. 
Mercury. 


I 

L  Pilocarpine. 


Lead. 


r  Syphilis I  Secondary. 

J  *.  Tertiary. 

(  Tuberculosis  (local). 


Simple  Local  Catarrhal  Stomatitis.  The  general  symptoms  of 
catarrhal  inflammation — heat  and  swelling,  with  deepened  color  of 
the  mucous  membrane,  followed  by  increased  secretion  and  exudation 
• — attend  several  types  of  oral  irritation,  such  as  the  irritation  induced 
by  erupting  teeth,  particularly  of  the  deciduous  teeth.  Inflammation 
of  any  degree  may  follow  the  taking  into  the  mouth  of  caustic  chemical 
substances,  such  as  caustic  alkalies,  mineral  acids,  carbolic  acid,  etc., 
which  are  occasionally  taken  by  children.  Other  irritant  drugs  and 
very  hot  fluids  may  produce  similar  results.  General  catarrhal  stoma- 
titis is  a  frequent  affection  of  confirmed  smokers,  and  of  drinkers  of 
distilled  liquors. 

The  cure  of  these  conditions  consists  in  the  removal  or  neutralization 
of  the  cause,  and  the  use  of  local  sedatives  and  antiseptics  to  allay 
irritation  and  prevent  infection.  The  most  effective  method  of  treat- 
ing the  inflammatory  condition  is  by  antiseptic  sprays,  such  as  diluted 
Dobell's  solution,  followed  by  sprays  of  strong  solutions  of  potassium 
chlorate.  If  much  pain  exist,  phenol-sodique  is  an  admirable  sedative 
antiseptic,  used  in  10-20  per  cent,  solution,  as  a  spray. 

Infective  Local  Catarrhal  Stomatitis.  This  in  some  degree  is  a 
common,  perhaps  the  necessary,  antecedent  condition  to  many  of  the 
ulcerative  forms  of  stomatitis.  It  is  probable  that  many  of  the  cases 
of  stomatitis  found  in  infants,  children,  and  adults  are  due  to  unusual 
fermentations  occurring  in  the  mouth.    Children  whose  nursing  bottles 


606  INFECTIONS  OF  AND  FROM  THE  MOUTH. 

are  not  kept  clean;  those  who  at  a  later  age  suffer  from  neglect  of  the 
teeth  and  from  the  effects  of  improper  food;  adults  in  whose  mouths 
dental  disease  is  widespread,  and  whose  oral  hygiene  is  very  faulty; 
all  exhibit  abnormal  conditions  of  the  oral  mucous  membrane — more 
or  less  swelling,  softness,  and  deepened  color  of  the  mucous  membrane, 
a  coated  tongue,  and  offensive  breath,  with  an  increase  of  oral  secretions. 

The  complexus  of  oral  symptoms  is  commonly,  and  also  by  the 
general  practitioner,  regarded  as  symptomatic  of  gastric,  intestinal,  and 
hepatic  disorders,  as  doubtless  they  are,  but  the  causal  relationship  is 
in  many  cases  probably  the  reverse  of  that  implied  in  such  opinions, 
for  it  is  probable  (see  later)  that  the  disturbances  of  digestion  are 
fermentative  in  character,  and  the  organisms  causing  them  find  their 
way  to  the  stomach  from  the  mouth,  which  was  first  affected.  The 
treatment  of  this  condition  consists  in  the  correction  of  its  causes, 
their  non-repetition,  and  the  continued  use  of  oral  antiseptics. 

While  the  point  of  first  attack  of  the  diphtheria  bacillus  is  most 
marked  about  the  soft  palate  and  tonsils,  the  false  membrane  forming 
there  and  spreading  to  the  pharynx,  more  or  less  general  inflammation 
of  the  oral  mucous  membrane  also  occurs.  The  gonococcus  may  be 
lodged  in  some  portion  of  the  oral  cavity  and  excite  its  specific  effects 
upon  contiguous  mucous  membranes. 

Symptomatic  Catarrhal  Stomatitis.  Stomatitis  in  its  catarrhal 
form  is  usually  associated  with  the  early  and  later  stages  of  the  eruptive 
fevers,  scarlet  fever,  smallpox,  etc.  In  scarlet  fever  and  smallpox 
evidences  of  direct  infection  of  the  mouth  exist  and  the  inflammatory 
reaction  is  pronounced. 

Catarrhal  stomatitis  is  one  of  the  manifestations  of  secondary  and 
tertiary  syphilis,  antedating  the  appearance  of  tissue  necrosis  (ulcera- 
tions). 

More  or  less  catarrhal  stomatitis,  confined,  it  may  be,  to  the  mucous 
membrane  of  the  gums,  is  common  in  the  mouths  of  phthisical  patients; 
this  condition  exhibits  no  evidence  of  direct  association  of  the  local 
development  of  the  bacillus  of  tuberculosis,  because  no  tubercular 
ulcers  may  arise  or  threaten. 

The  stomatitis  of  typhoid  fever  may  be  regarded  as  an  almost 
essential  feature  of  the  disease. 

The  effects  of  drug  elimination  by  the  oral  tissues  have  been  already 
discussed.     (See  Chapter  XXIII.) 

Ulcerative  Stomatitis.  It  has  been  customary  to  describe  ulcerative 
stomatitis  as  simple  and  infective;  in  all  probability  these  ulcerations 


STOMATITIS.  607 

are  always  infective.  Like  catarrhal  stomatitis  the  ulcerative  disease 
may  have  only  a  local  significance  or  be  indicative  of  some  general 
disease. 

Ulcerative  Stomatitis  of  Local  Significance.  The  more  usual  or 
infantile  forms  of  these  disorders  are  a  sequel  of  catarrhal  stomatitis, 
at  least  of  an  acquired  debility  of  the  oral  tissues,  and  their  primary 
cause  is,  therefore,  the  cause  producing  a  condition  of  mucous  mem- 
brane which  permits  the  growth  of  infective  organisms.  One  of  these 
diseases,  thrush,  has  already  been  described.  The  others,  aphthse, 
herpes  labialis,  and  noma,  are  all  probably  due  to  the  action  of 
organisms. 

Aphthae.  This  affection  is  common  in  its  isolated  form,  as  the 
canker  sore.  In  the  catarrhal  stomatitis  of  children,  during  or  after 
dentition,  multiple  sores  frequently  make  their  appearance.  The  con- 
dition can  best  be  studied  when  it  appears  as  an  isolated  sore  in  the 
mouth  of  the  adult.  The  most  common  situation  of  the  sore  is  at  the 
junction  of  two  mucous  surfaces,  such  as  that  of  the  gum  with  the  lip 
or  cheek,  or  that  of  the  floor  of  the  mouth  with  the  gum  or  tongue. 
Redness  diffused  over  a  limited  area,  followed  by  a  nodular  hardening, 
occurs,  during  which  local  pain  is  annoying;  the  centre  of  the  hardened 
area  breaks,  the  epithelium  disappearing,  forming  a  raw  surface,  which 
quickly  acquires  a  rough,  yellowish-white  coating  which  is  easily 
removable.     The  sores  are  very  painful. 

The  mouth  is  usually  otherwise  healthy,  and  there  is  an  absence  of 
associated  throat  and  skin  affections. 

This  condition  follows  so  constantly  upon  the  taking  of  very  indi- 
gestible food,  such  as  lobster,  Welsh  rarebits,  etc.,  that  acute  indigestion 
must  be  regarded  as  having  some  causal  relationship  with  it.  It  is  also 
of  frequent  occurrence  in  the  mouths  of  dyspeptics;  that  form  of 
gastric  disturbance  attended  by  a  deficiency  of  hydrochloric  acid  in  the 
gastric  juice  appears  to  have  a  constant  association  with  it,  though  it 
is  probably  caused  by  the  oidium  albiccins. 

The  appearance  of  ulcerative  stomatitis  in  children,  together  with 
its  treatment,  was  discussed  in  the  chapter  on  Dentition. 

The  general  treatment  of  these  ulcerations  appearing  in  the  mouths 
of  children  is  the  administration  of  a  laxative,  and  the  subsequent 
administration  of  listerine,  gtt.  x,  every  two  hours.  Locally  the 
mucous  membrane  is  to  be  sprayed  with  pyrozone,  followed  by  sprays 
of  strong  solutions  of  potassium  chlorate. 

Localized  aphthous  patches  in  the  adult  are  promptly  relieved  by 


608 


INFECTIONS  OF  AND  FROM  THE  MOUTH. 


the  administration  of  calomel,  gr.  ij,  at  night,  followed  in  the  morning 
by  a  mild  saline.  The  local  sore  is  dried  and  touched  with  pure 
carbolic  acid.  The  administration  of  alkalies  before  meals,  and 
hydrochloric  acid  after  meals,  usually  remedies  the  gastric  condition, 
unless  it  be  of  long  standing. 

A  variety  of  aphthous  sore  is  called,  from  the  anatomical  situation 
of  the  ulcers,  follicular  stomatitis.  Irritation  and  swelling  of  the 
mucous  follicles  in  the  palatal,  buccal,  and  labial  mucous  membrane 
are  accompanied  by  more  or  less  localized  inflammation;  the  follicles 
become  ulcerous,  the  small  ulcers  having  a  uniform  size.  This  con- 
dition quickly  disappears  under  the  treatment  advised  for  ulcerative 
stomatitis.  An  indication  of  the  bacterial  origin  of  all  of  these  dis- 
turbances is  seen  in  the  efficacy  of  antiseptics  used  in  their  treatment. 

NOMA,    CANCRUM   ORIS,    GANGRENE   OF   THE   MOUTH. 

In  ill-fed,  ill-nourished,  and  ill-kept  cachectic  children,  the  debilita- 
tion of  the  oral  tissues  may  exceed  the  grades  given,  and  a  disease, 

Fig.  543. 


Noma.    (J.  Lewis  Smith.) 


probably  bacterial  in  origin,  may  arise  which  leads  to  widespread 
necrosis  of  the  cheeks  and  maxillse.    The  condition  is  called  gangrene 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH.  609 

of  the  mouth,  noma,  or  cancriim  oris;  the  latter  term  has  been  applied 
to  the  less  severe  varieties. 

This  disease  may  make  its  appearance  as  an  ulcer  at  the  junction 
of  cheek  and  gum;  in  other  cases  a  severe  stomatitis  arises  without  a 
primary  ulcer.  A  greater  or  less  extent  of  the  cheek  acquires  a  board- 
like hardness,  becoming  livid ;  the  overlying  mucous  membrane  breaks, 
exhibiting  a  large  slough.  The  necrosis  extends  toward  cheek  and  jaw, 
destroying  further  tissue.  The  sloughs  undergo  putrefactive  decom- 
position, emitting  a  stench.  The  destruction  of  tissue  may  be  arrested, 
or  may  proceed,  destroying  in  a  few  days  the  entire  cheek  and  bony 
tissues.  In  the  more  severe  cases  the  disease  is  almost  invariably  fatal, 
because  the  extent  of  the  tissue  destruction  bears  a  constant  relation  to 
the  underlying  debility  of  the  patient.  It  will  be  seen  that  the  disease 
resembles  malignant  pustule  or  carbuncle  in  several  of  its  features. 

While  no  specific  organism  has  been  isolated  as  pathogenic  of  this 
condition,  Schimmelbosch^  found  a  bacillus  (pure  culture)  upon  the 
borders  of  the  necrosis,  which  may  prove  pathogenic  of  noma. 

These  cases  are  purely  medical;  so  that  their  full  discussion  is  not 
warranted  in  these  pages.  The  principle  of  treatment  is  to  improve 
the  general  condition  of  the  child,  destroy  the  probable  infection  in  the 
borders  of  the  still  vital  tissue  by  cauterization,  and  promote  sloughing 
of  the  necrosed  tissue  by  the  use  of  antiseptic  applications. 

Dr.  L.  Fisher  (New  York)  reported  a  case  upon  the  inside  of  the 
cheek,  cured  by  applications  of  ichthyol  in  lanolin  four  times  a  day 
over  the  entire  area." 

SYPHILITIC  AFFECTIONS  OF  THE  MOUTH. 

The  recognition  of  syphilitic  lesions  about  the  mouth  is  of  vital 
importance  to  the  dental  operator,  first,  because  by  the  recognition 
he  may  take  steps  to  prevent  the  carriage  of  infection  to  innocent 
patients;  and,  secondly,  that  he  may  avoid  inoculation  of  himself  by 
the  poison. 

In  the  minds  of  many,  syphilis  is  associated  with  the  lower  class  of 
persons,  who  are  confirmed  debauches.  While  it  is  undoubtedly  true 
that  its  prevalence  is  most  marked  in  this  class  of  persons,  it  appears, 
and  with  horrible  frequence,  in  persons  who  would  be  little  suspected 
of  having  such  infection.  The  operator  is  to  be  guided  in  his  opinions 
and  precautions  in  this  matter,  not  by  the  social  status  of  the  patient, 
but  by  the  nature  of  the  morbid  conditions  existing. 

1  Miller,  Dental  Cosmos,  September,  1891.  -  Dental  Cosmos,  1902. 

39 


610  INFECTIONS  OF  AND  FROM  THE  MOUTH. 

Syphilis  is  usually  divided  into  three  stages,  primary,  secondary,  and 
tertiary;  to  these  may  be  added  a  fourth,  stage,  viz.,  in  patients  who 
have  been  discharged  as  cured  mild  manifestations  of  disorders,  par- 
ticularly of  the  skin  and  mucous  membranes,  make  their  appearance 
from  time  to  time,  and  disappear  promptly  upon  the  administration  of 
iodides. 

The  first  stage  of  syphilis — primary  syphilis — consists  in  the  forma- 
tion of  the  primary  sore  or  chancre,  and  the  involvement  of  the  nearest 
lymphatic  glands.  Secondary  syphilis  is  attended  by  fever,  eruptive 
inflammations  of  the  skin,  inflammation  and  superficial  ulcerations  of 
mucous  structures.  In  tertiary  syphilis  destructive  inflammation  of 
the  skin,  mucous  membranes,  and  connective  tissue  occurs,  together 
with  the  formation  of  specific  tumors — gummata. 

Some  difference  of  opinion  exists  among  syphilographers  as  to  the 
relative  infective  power  of  the  secretions  from  the  several  lesions 
of  syphilis.  All  are  agreed,  however,  that  the  secretions  from  the 
secondary  lesions  observed  in  and  about  the  mouth  are  highly  infective. 
It  is  the  part  of  prudence  to  regard  all  syphilitic  lesions  as  infective. 
All  these  stages  of  syphilis  may  be  seen  in  the  human  mouth.  It  is  to 
be  remembered  that  if  the  mucous  membrane  of  the  mouth  be  infected 
from  a  mucous  patch  (a  secondary  lesion),  the  acquired  disease  will 
appear,  not  as  a  mucous  patch,  but  as  a  chancre.  It  is  from  mucous 
patches  that  infection  is  most  to  be  feared. 

Primary  Syphilis  of  the  Mouth.  Causes.  The  primary  lesion 
of  syphilis,  chancre,  when  found  in  the  mouth  is  a  consequence  of 
direct  infection  from  a  syphilitic.  The  infection  occurs  from  contact 
of  the  mucous  surface  of  the  mouth  with  a  syphilitic  lesion  upon 
another  person:  it  has  been  transmitted  by  kissing;  it  may  occur  from 
using  a  glass  or  cup  previously  used  by  a  syphilitic,  by  smoking  cigars 
or  cigarettes  which  have  been  made  by  syphilitic  cigarmakers,  who 
have  applied  the  tongue  to  the  tobacco  in  attaching  the  wrapper.  Any 
of  the  articles  named,  or  the  contact  of  any  article  which  has  been  in 
contact  with  a  syphilitic  lesion,  if  brought  in  contact  with  an  abraded 
mucous  surface  may  cause  infection. 

The  infection  may  be  transferred  from  patient  to  operator  if  the 
fingers  have  any  abraded  surface,  or  if  the  surface  is  broken  accident- 
ally by  an  instrument.  Infection  may  be  transmitted  from  one  patient 
to  another  by  any  instrument,  appliance,  or  article  used  by  a  syphilitic 
being  afterward  used  by  an  innocent  person.  Drinking  glasses,  mouth 
mirrors,    exploring    instruments,    rubber-dam,    rubber-dam    clamps. 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH.  611 

saliva-ejector  tubes,  lancets,  forceps,  or  any  other  instruments  may 
be  the  medium  of  communication.  During  and  since  the  time  of 
Hunter  the  use  of  teeth  from  syphilitic  patients  in  plantation  opera- 
tions has  been  a  clearly  recognized  medium  of  communication. 

Appearances  and  Diagnosis.  "The  primary  lesion  of  syphilis  never 
makes  its  appearance  before  ten  days  after  infection;  the  maximum 
period  is  about  ninety  days;  the  average  is  twenty-one  days."^ 

It  usually  appears  as  a  single,  elevated,  hard  papule.  In  cases  of 
dental  infection,  most  frequently  about  the  lips,  the  papule  loses  its. 
epithelial  coating  after  some  days.  The  induration  surrounding  the 
papular  mass  increases  until  the  papule,  which  is  now  raw  and  in  a. 
process  of  ulceration,  appears  surrounded  by  a  ring  of  cartilaginous^ 
hardness.  This  induration  is  the  one  distinguishing  feature  of  the 
chancre,  which  is  not  painful.  In  about  a  week  after  the  appearance 
of  the  primary  sore,  swelling  of  the  submaxillary  lymphatic  glands  is 
observed.  In  case  the  chancre  appear  upon  the  tongue,  the  subhyoid 
lymphatic  glands  are  swollen.^  Unless  pyogenic  infection  have  occurred 
the  lymphatic  involvement  is  not  inflammatory,  there  being  no  pain 
present.  In  from  three  to  four  weeks  the  sore  disappears,  leaving  no 
signs  of  its  site  in  some  cases;  in  others,  some  induration  may  persist. 

The  diagnosis  of  this  condition  is  the  important  consideration,  so  far 
as  the  dental  practitioner  is  concerned,  its  treatment  being  the  province 
of  the  general  surgeon. 

The  elevation  of  the  sore,  its  induration,  and,  if  obtainable,  the  time 
of  inoculation,  are  diagnostic  data.  The  sore  is  single,  and  there  is 
hard,  nodular,  painless  swelling  of  the  neighboring  lymphatics.  A 
single  ulcer  of  ulcerative  stomatitis  may  in  some  degree  simulate  the 
appearance  of  a  very  small  chancre.  It  may  exhibit  slight  induration, 
but  its  irregular  form,  situation,  painfulness,  and  the  usual  absence 
of  lymphatic  involvement,  together  with  its  prompt  disappearance 
after  sterilizing  the  mouth  and  cauterizing  the  ulcer,  will  differentiate 
the  two  sores.  If  the  chancre  be  upon  the  tip  or  sides  of  the  tongue, 
where  it  is  subjected  to  irritation,  it  may  become  very  large  and  bear 
a  close  resemblance  to  epithelioma  of  that  organ. 

It  is  a  wise  precaution  to  view  all  sores  about  the  mouth  as  possibly 
infectious.  All  errors  of  diagnosis  in  this  direction  will  be  more  than 
compensated  for  by  the  assurance  of  non-transference  of  infection. 

Secondary  Syphilis  of  the  Mouth.  The  secondary  manifestations 
of  syphilis  are  observed  in  and  about  the  mouth,  no  matter  what  the 

1  Grossi  System  of  Surgery.  -  -  Park,  Surgery. 


612 


IXFECTIONS  OF  AND  FROM  THE  MOUTH. 


Fig.  544. 


location  of  the  primary  lesion  may  have  been;  they  are  the  result  of 
a  general,  not  a  local,  infection. 

Secondary  affections  of  the  mucous  tissues  appear  in  from  four  to 
twelve  weeks  after  the  appearance  of  the  primary  lesion.  Sore  throat, 
due  to  inflammation  of  the  mucous  membrane  of  the  phar^nix  and  parts 
about,  is  almost  constant;  together  with  syphilitic  hoarseness,  due  to 
the  extension  of  the  affection  to  the  mucous  membrane  of  the  larynx. 
The  appearance  of  copper-colored  areas  upon  some  portion  of  the 
mucous  membrane,  on  the  tonsil,  pharynx,  soft  palate,  lips,  or  bucco- 

labial  surface,  precedes  the  loss 
of  epithelium  over  these  surfaces, 
which  soon  occurs,  forming  the 
most  virulently  contagious  lesion 
of  syphilis,  the  mucous  patch. 
The  patches  become  covered  with 
a  grayish-white,  pasty  covering, 
resembling  the  ulcerations  of  non- 
specific stomatitis.  So  close  is 
the  resemblance  that  a  differen- 
tiation can  only  be  made  at  times 
by  additional  evidences  of  second- 
ary syphilis.  Single  patches  may  coalesce,  forming  large,  irregular 
areas  covered  by  a  grayish- white  pellicle.  These  patches  are  rarely 
painful.  Ulcerations  having  ragged,  irregular  outlines  may  appear  at 
the  sites  of  the  original  patches  or  in  other  situations,  and  exhibit  a 
tendency  to  spread. 

The  diagnosis  of  the  condition  is  determined  by  a  discovery  of  other 
lesions  of  secondary  syphilis;  skin  eruptions,  falling  out  of  the  hair 
(alopecia),  and  the  areas  of  copper-colored  eruption  upon  the  mucous 
membrane  of  the  pharynx  and  soft  palate. 

Hugenschmidt^  has  observed  among  syphilitics,  w^ho  presented  no 
local  lesions,  the  frequent  nocturnal  occurrence  of  indefinitely  located 
dental  pains,  spreading  to  the  palatal  region. 

Tertiary  Syphilis  of  the  Mouth.  The  syphilides  of  the  secondary 
stage  arise  in,  and  are  confined  to,  the  mucous  and  dermal  structures; 
those  of  the  tertiary  stage  arise  in  the  deep  connective  tissues,  and 
are  frequently  associated  with  periosteum. 

Tertiary  lesions,  as  seen  by  the  dentist,  are  usually  in  the  form  of 
ulcers  of,  first,  the  soft  or  hard  palate,  and  of  the  tongue  or  lips.     In 


Chancre  of  the  lip. 


1  Dental  Cosmos,  1892. 


TUBERCULOSIS  OF  THE  MOUTH.  613 

the  earlier  stages  hard,  nodular  formations  may  be  noted  as  ante- 
cedents to  the  ulcerations.  Chronic  periostitis  of  the  palatal  processes 
may  occur,  leading  to  the  formation  of  localized  thickenings.  In  other 
cases,  in  the  soft  palate,  upon  the  tongue,  or  in  the  hard  palate,  local- 
ized swellings  may  occur;  the  overlying  mucous  membrane  breaks, 
establishing  an  ulcer,  which  may  perforate  the  soft  palate  and  destroy 
a  portion  of  the  palataL  process,  or  form  large  ulcers  on  the  tongue. 
These  lesions  appear  in  from  two  to  five  years  after  the  secondary 
manifestations. 

Although  there  is  much  doubt  as  to  the  degree  of  infectiveness  of 
these  tertiary  lesions,  precautions  as  to  sterilization  should  be  taken  as 
with  the  primary  and  secondary  lesions.  A  defined,  ragged  ulcer 
occupying  the  hard  or  soft  palate,  which  has  persisted  for  a  long  time, 
should  always  be  viewed  with  suspicion,  and  a  search  be  made  for 
other  evidences  of  syphilis. 

These  ulcerations  appearing  upon  the  side  of  the  tongue  may  closely 
simulate  epithelioma  of  that  organ.  The  confusion  is  increased  if,  in 
consequence  of  the  presence  of  jagged  teeth,  a  continuous  irritation  is 
excited.  Moreover,  leukoplakia  of  the  cheeks,  a  diagnostic  sign  of 
incipient  epithelioma,  frequently  accompanies  tertiary  syphilis.  In 
some  cases  an  absolute  diagnosis  is  only  made  by  noting  the  disappear- 
ance of  the  local  lesion  following  the  administration  of  iodides,  the 
specific  treatment  of  tertiary  syphilis. 

The  existence  of  tertiary  syphilis  is  of  great  clinical  importance  to 
the  dentist  in  that  a  condition  of  lessened  resistance  of  tissues  is  estab- 
lished, and  disease  processes  which  in  the  healthy  person  are  compara- 
tively circumscribed,  in  the  syphilitic  run  a  riotous  course.  A  septic 
pericementitis  by  extension  may  involve  a  wide  area  of  periosteum, 
leading  to  extensive  maxillary  necrosis. 

TUBERCULOSIS  OF  THE  MOUTH. 

The  bacillus  of  tuberculosis,  under  favorable  conditions,  develops  in 
the  tissues  of  the  mouth,  producing  its  characteristic  lesions.  Finding 
a  suitable  soil,  such  as  is  furnished  by  the  heredity  which  predisposes 
to  phthisis  pulmonalis,  the  bacillus  may  find  entrance  to  the  deeper 
tissues  from  the  mucous  membrane  of  the  mouth  and  excite  tuber- 
culosis in  the  deep  structures,  the  bone,  etc.  What  part  is  played  by 
local  oral  and  dental  lesions  in  tuberculosis  of  distant  parts,  by  estab- 
lishing pathways  for  the  entrance  of  the  bacilH  into  the  circulation,  is 
at  present  conjectural,  but  that  such  infections  occur  is  very  probable. 


614  INFECTIONS  OF  AND  FROM  THE  MOUTH. 

ACTINOMYCOSIS. 

The  condition  produced  bv  the  development  of  the  ray-fungus,  the 
actinomycosis,  in  the  lower  jaw  and  cervical  regions  of  cattle  and 
swine— lump-jaw — is  not  unknown  in  human  beings. 

Miller^  gives  203  cases  reported  in  German  medical  literature 
between  1886  and  1891.  In  at  least  120  of  these  cases  the  point  of 
entrance  of  the  fungus  was  found  to  be  in  the  region  of  the  mouth  or 
throat.  Actinomycosis  threads  have  been  repeatedly  found  in  the 
saliva  and  in  carious  teeth,  and  notably  in  the  tonsils.  Whether  the 
path  of  entrance  to  deeper  structures  is  ever  through  carious  teeth  is 
undetermined,  but  certainly  lesions  or  wounds  about  the  mouth 
furnish  an  entrance. 

GONORRH(EA. 

Undoubted  cases  of  oral  infection  by  the  gonococcus  of  Neisser 
have  occurred.  The  oral  mucous  membrane  and  the  gums  may 
undergo  intense  suppuration.  Fever  and  its  accompaniments  may 
be  present.  The  mouth  and  eyes  are  very  subject  to  secondary  infec- 
tion in  an  individual  suffering  from  gonorrhceal  urethritis.  The 
toxins  and  the  germs  formed  in  the  mouth  may  be  swallowed. 

GENERAL  SEPTIC  DISEASES  OF  DENTAL  ORIGIN. 

The  effect  of  the  existence  of  dental  diseases  upon  the  body  at  large, 
particularly  as  regards  secondary  infection,  is  a  matter  increasing  in 
importance  as  the  possibilities  of  their  connection  are  made  out.  At 
present,  the  organisms  of  greatest  demonstrable  pathological  interest 
are  the  pyogenic  cocci.  The  almost  constant  presence  of  these 
organisms  in  the  mouth,  carried  thence  into  the  pharynx,  posterior 
nares,  larynx,  lungs,  and  stomach,  furnishes  the  reason  for  the  pyogenic 
and  phlegmonous  inflammations  which  occur  in  these  organs.  The 
diplococcus  of  penumonia,  a  frequent  organism,  but  waits  a  favorable 
opportunity  to  establish  high  inflammations  and  fibrinous  exudations 
in  the  lungs,  and  possibly  in  other  structures. 

The  most  important  chnical  associations  of  dental  with  general 
infections  are  diseases  of  the  pericementum.  The  pulps  of  teeth, 
having  no  lymphatics,  do  not  appear  to  take  up  and  transmit  the 
products  of  the  action  of  septic  organisms;  but  while  the  evidences 

1  Dental  Cosmos,  1891. 


DENTAL  STERILIZATION.  615 

of  such  absorption,  involvement  of  the  neighboring  lymphatics,  are  not 
present,  it  must  be  remembered  that  the  veins  may  transmit  the  poison, 
and,  in  addition,  may  perhaps  convey  organisms  from  a  diseased  but 
still  vital  pulp  to  distant  parts.  When,  however,  the  pulp  is  dead  and 
the  pericementum  is  invaded,  there  is  no  doubt  of  general  infection 
from  this  local  source.  INIore  or  less  septic  intoxication  is  a  common 
attendant  upon  severe  septic  apical  pericementitis,  and  septicaemia 
accompanied  by  inflammation  of  the  neighboring  Ijonphatic  glands  is 
of  sufficient  frequency  to  emphasize  the  need  of  the  vigorous  antiseptic 
treatment  recommended  in  all  of  these  cases. 

Pyaemia  is  far  more  uncommon,^  Pyogenic  organisms,  gaining 
access  to  the  blood  current  from  the  local  source  of  infection,  establish 
suppuration  in  distant  parts;  in  other  parts  of  the  bone,  or  in  other 
bones  (osteomyelitis),  in  the  lungs,  meninges,  and  substance  of  the 
brain.  One  case^  has  been  reported  where  abscess  of  a  toe,  ear,  and 
forearm  ceased,  and  recovery  took  place  after  treatment  and  filling  of 
septic  root  canals.  Several  cases  are  tabulated  by  the  same  author 
in  which  extensive  necrosis  and  death  resulted  from  pysemic  infection 
from  septic  pericementitis.  Some  of  these  cases  recorded  were  asso- 
ciated with  acute,  some  with  chronic  septic  pericementitis. 

In  addition  to  the  usual  pyogenic  cocci.  Miller  has  isolated  several 
forms  of  cocci,  bacilli,  and  spirilla,  forming  products  which,  if  injected 
into  the  circulation  of  animals,  cause  death  from  septicaemia  in  from 
hours  to  days.  As  many  of  these  forms  may  be  brought  into  relation 
with  deep  parts  by  the  anatomical  conditions  created  by  pulp  death, 
the  possibiUties  of  many  types  of  infection  ma  pulpless  teeth  are 
evident. 

The  possibilities  of  local  as  well  as  general  infections  through  the 
conditions  established  in  the  several  forms  of  pyorrhoea  alveolaris 
should  not  be  forgotten. 

The  pockets  formed  by  the  soft  tissues  overhanging  lower  third 
molars  whose  eruption  is  impeded  invite  the  passage  of  septic  organ- 
isms to  deep  parts.  Local  pyogenic  infections  are  common  in  these 
cases. 

DENTAL  STERILIZATION. 

It  must  ever  be  borne  in  mind  that  the  dental  operator  constantly 
works  in  a  field  of  infection,  and  unless  extraordinary  precautions  be 
taken  every  instrument  which  touches  this  field — the  fingers  of  the 

1  Miller,  Dental  Cosmos,  1891.  2  Ibid. 


616  INFECTIONS  OF  AND  FROM  THE  MOUTH. 

operator,  his  mirrors,  glasses,  napkins,  rubber-dam,  rubber-dam 
clamps — becomes  immediately  infected  as  soon  as  it  is  brought  in 
contact  with  the  mouth  of  the  patient.  The  likelihood  of  infection 
varies  with  the  patient  and  the  particular  instruments;  mouth-mirrors, 
rubber-dam  clamps,  scalers,  and  all  instruments  used  in  the  treatment 
of  pulp  canals  are  likely  to  become  more  promptly  and  extensively 
infected  than  other  instruments.  Again,  the  forms  of  the  instruments 
determine  whether  or  not  increased  opportunity  is  given  for  the  reten- 
tion of  infective  material.  The  fingers  of  the  operator  may  be  the 
medium  through  which  infective  material  is  transferred  from  one 
patient  to  another.  Infection  may  be  carried  from  superficial  areas 
of  the  mucous  membrane  of  the  mouth,  from  the  enamel  and  the 
saliva,  into  deeper  structures,  where  conditions  are  favorable  for  the 
development  of  sepsis. 

The  scheme  for  dental  sterilization,  therefore,  includes  the  steriliza- 
tion of  the  operator,  instruments,  apparatus,  appliances,  etc.,  used  in 
operations,  and  the  sterilization  of  the  field  of  operation  prior  to 
operating. 

The  Operator.  Extreme  personal  cleanliness  upon  the  part  of  an 
operator  is  clearly  the  first  step  in  asepsis.  The  best  class  of  dentists 
are  exceedingly  neat  as  regards  personal  habits:  daily  bathing,  care  of 
the  nails  and  of  the  skin,  and  immaculate  linen  form  as  much  a  part 
of  the  day's  labor  as  dental  operations  per  se.  The  virtues  of  soap 
and  water,  wherever  they  may  be  applied,  are  regarded  as  a  very 
important  item  in  preventing  infection. 

Linen  which  has  been  boiled  prior  to  wearing  may  be  regarded  as 
safely  sterile;  so  that  the  matter  of  personal  sterilization  relates  to  the 
hands,  particularly  to  the  finger-nails.  The  space  under  the  nails  is  a 
favorable  habitat  for  many  organisms,  notably  the  pyogenic  cocci,  the 
staphylococcus  pyogenes  aureus  being  commonly  present  in  this 
situation. 

It  has  always  been  advised  that  the  finger-nails  be  trimmed  short, 
and  be  made  smooth  to  avoid  mechanical  injury  to  the  soft  tissues  of 
the  patient.  Since  the  advent  of  aseptic  and  antiseptic  surgery  these 
precautions  have  an  additional  significance;  nails  kept  short  and 
smooth  may  be  more  readily  cleansed  than  if  long  and  ill-kept.  The 
nails  should  be  cut  so  that  they  nowhere  project  beyond  the  tips  of 
the  fingers.  Their  mechanical  cleansing  should  be  done  with  smooth 
instruments,  not  sharp  knife-blades;  the  latter  produce  rough  surfaces, 
which  furnish  spaces  for  lodgement  of  bacteria.     There  is  but  one 


DENTAL  STERILIZATION.  617 

effective  method  of  washing  beneath  the  nails;  it  is  that  followed  by 
the  general  surgeon:  after  dipping  the  soap  in  water  as  hot  as  can  be 
borne  by  the  hands,  all  of  the  finger-nails  should  be  made  to  scrape  the 
soap  until  the  spaces  under  the  nails  are  filled  with  soap.  After  this, 
coarse  hand-brushes  are  used  to  scour  every  part  of  the  hands  with 
soap  and  water  as  hot  as  can  be  borne.  Special  nail-brushes  are  next 
used  to  scrub  beneath  the  nails,  driving  out  piecemeal  the  soap  masses 
there.  The  general  surgeon  continues  the  scrubbing  until  the  nails 
are  scrupulously  clean.  The  soap  usually  used  is  Castile,  or  soap 
made  from  palm  oil,  etc. ;  but  antiseptic  soaps,  such  as  ethereal  soaps, 
may  be  substituted  with  advantage. 

Sterilization  of  the  cleansed  hands  is  ensured  by  immersing  them 
for  five  minutes  in  antiseptic  solutions,  such  as  a  1 :  2000  solution  of 
mercuric  chloride.  The  hands  should  be  sterilized  after  treating  each 
patient;  rubbing  the  hands  with  a  paste  of  flour  of  mustard  and  water 
for  three  minutes  and  washing  off  with  sterilized  water  is  effective 
(Nancrede).  If  the  patient  dismissed  have  possessed  an  unusually 
septic  mouth,  or  have  been  a  syphilitic,  for  example,  the  time  for 
hand  cleansing  and  sterilization  is  to  be  prolonged;  if  syphilitic,  every 
instrument  used  is  transferred  to  separate  vessels  containing  antiseptic 
solutions  or  boiled,  and  the  hands  are  viewed  as  highly  infected; 
they  are  scrubbed  with  mercuric  chloride  solutions  to  prevent  personal 
infection  or  the  carriage  of  infection.  Chancres  have  from  time  to  time 
appeared  upon  the  fingers  of  dentists  as  well  as  physicians. 

Sterilization  of  Apparatus.  The  scrupulous  cleanliness  of  the 
operating  chair,  whose  head-rest  should  receive  frequent  changes  of 
boiled-linen  coverings,  metallic  parts  rubbed,  and  general  covering 
cleansed;  the  cleansing,  polishing,  and  sterilizing  of  cuspidores;  the 
changing  of  paper  coverings  upon  instrument  tables,  etc.,  are  part  of 
the  general  scheme  of  sterilization.  The  floor  of  the  operating  room 
also  requires  attention;  instead  of  being  covered  with  carpet,  it  is 
preferable  to  have  it  made  of  parquetry  material  or  cement,  over  which 
rugs  are  laid,  which  may  be  removed  from  the  room  for  cleansing, 
the  floor  proper  being  scrubbed. 

Napkins  used  about  the  mouth  are  certain  to  become  infected,  so 
that  their  boiling  should  be  prolonged  at  least  fifteen  minutes.  For 
many  operations  it  is  preferable  to  substitute  strips  of  muslin  for  linen 
napkins,  which  after  being  used  may  be  thrown  away. 

If  a  hydraulic  saliva  ejector  be  used,  the  glass  mouth-tubes  should 
be  changed  for  each  person,  a  sterilized  tube  being  substituted  directly 


618  IXFECTIOXS  OF  AXD  FROM  THE  MOUTH. 

before  its  use  is  required.  A  number  of  these  tubes  should  be  in  use 
and  may  be  sterihzed  after  washing  by  placing  them  in  a  50  per  cent, 
solution  of  listerine  or  in  5  per  cent,  formaldehyde  for  a  few  hours. 
Tumblers  and  mouth-mirrors  may  be  sterilized  in  like  manner.  The 
cloudiness  of  saliva  tubes  is  produced  by  the  formation  of  salivary 
calculus,  and  may  be  removed  by  the  use  of  acidulated  water.^ 

At  the  close  of  each  day  a  large  cup  should  be  filled  with  an  anti- 
septic solution,  which  is  to  be  drawn  through  the  tubing  of  the  ejector 
to  keep  it  in  a  reasonably  aseptic  condition. 

Rubber-dam  may  be  sterilized  by  boiling  water,  but  it  is  more  safe 
and  cleanly  to  use  a  new  piece  for  each  patient.  It  should  be  washed 
and  then  dusted  mth  borated  talcum  powder.  The  possibilities  of 
infection  through  this  medium  are  great,  particularly  in  syphilitic 
cases. 

Sterilizing  Instniments.  The  sterilizing  of  instruments  comprises 
their  mechanical  cleansing  and  the  use  of  germicides;  boiling  water, 
formaldehyde  vapor,  and  antiseptic  drugs  are  all  employed  for  this 
purpose.  The  former,  being  the  most  convenient  and  certain  sterilizing 
agent,  is  used  wherever  it  cannot  produce  injury  to  instruments. 

Nancrede'  states  that  all  pyogenic  cocci,  and  even  anthrax  spores, 
are  killed  by  boiling  instruments  for  two  minutes  in  a  1  per  cent, 
solution  of  sodium  carbonate,  which  also  prevents  rusting. 

All  instruments  should  be  kept  in  a  highly  polished  condition,  being 
rubbed  with  crocus  cloth  at  the  end  of  each  day's  use.  Excavators, 
explorers,  and  pulp-canal  cleansers  should  be  mechanically  freed  from 
visible  foreign  matter  before  boiling,  by  rubbing  their  points  with  a 
cocoa-fibre  or  wire  brush.  A  fibre  brush  should  be  used  to  cleanse 
all  excavating  burs  which  have  been  in  use.  The  brush  should  also 
be  boiled  daily  and  especially  after  an  unusually  infective  case.  It 
is  good  practice  to  permit  it  to  lie  in  a  5  or  10  per  cent,  solution  of 
formaldehyde. 

Mouth-mirrors,  of  which  there  should  be  several,  require  special 
care.  Their  edges  afford  favorable  lodging  places  for  bacteria,  and 
require  careful  sterilization.  Miller^  found  that  the  usual  antiseptic 
solutions  used  cold  acted  as  very  imperfect  sterilizers,  but  at  the 
temperature  of  boiling  their  eflacacy  was  markedly  increased. 

Extracting  forceps  require  careful  mechanical  cleansing  and  pro- 
longed boihng  after  each  use,  for  perhaps  more  cases  of  infection, 

1  Thornton,  Dental  Review,  1903.  -  Park's  Surgery  by  American  Authors. 

s  Dental  Cosmos,  1891. 


DENTAL  STERILIZATION. 


619 


and  of  many  kinds,  have  resulted  from  unclean  forceps  than  from 
all  other  causes  combined. 

Instruments,  such  as  hand-pieces  which  cannot  be  conveniently 
boiled,  may  be  subjected  for  ten  minutes  to  formaldehyde  gas, 
developed  in  a  Low  or  Schering  apparatus/  If  desired,  all  the  in- 
struments may  be  so  sterilized.  The  entire  instrument  case  may  be 
disinfected  by  burning  a  Low  lamp  in  one  drawer  of  the  dental  cabinet 
for  a  half-hour  at  night.  The  drawers  should  be  made  communicating 
by  small  perforations  at  one  or  more  points. 

Sterilizing  the  Field  of  Operation.  To  ensure  sterihzation  of  the 
field  of  operation  antiseptics  should  be  used  freely  about  the  mouth 

Fig.  545. 


Low  sterilizer:  A,  sterilizing  chamber;  B,  perforated  tray  on  which  instruments  to  be  sterihzed 
are  placed;  C,  glass  dome  and  cast  aluminium  support,  O,  forming  condensing  chamber  for 
removing  all  moisture  from  gas;  D,  formaldehyde  bxirner;  E,  platinimi  cone,  which  generates  the 
gas  from  Columbian  spirit;  F,  lamp  body.  The  course  of  the  gas  through  the  apparatus  is  indi- 
cated by  the  arrows. 

prior  to  operating.  The  thoroughness  of  the  sterilization  will  depend 
in  great  degree  upon  the  personal  habits  of  the  patient.  If  by  the 
systematic  use  of  the  agents  and  measures  described  under  the  prophy- 
laxis of  caries  the  patient's  mouth  be  kept  in  a  reasonably  aseptic 
condition,  sterilization  of  the  oral  cavity  can  be  accomplished  with 
sufficient  readiness.  The  choice  of  antiseptic  will  depend  in  great 
degree  upon  the  state  of  oral  hygiene;  in  ill-kept  mouths,  with  deposits 
of  foreign  materials  about  and  between  the  teeth,  on  the  gums  and 
tongue,  much  more  active  and  penetrating  germicides  will  be  required 
than  if  the  parts  are  clean.  The  presence  of  putrefactive  decom- 
position in  the  mouth,  made  evident  by  ill  odors,  amid  which  that  of 
hydrogen   sulphide   may   be   detected,    needs   for   its   treatment  the 


1  See  American  Text -book  of  Operative  Dentistry. 


620  INFECTIONS  OF  AND  FROM  THE  MOUTH. 

immediate  and  free  use  of  preparations  from  which  nascent  chlorine 
or  nascent  oxygen  may  be  disengaged.  No  operation  or  even  examina- 
tion should  be  begun  in  such  cases  before  a  claret-colored  solution  of 
potassium  permanganate,  or  a  strong  solution  of  hypochlorites  (medi- 
trina  diluted),  has  been  freely  used  by  the  patient.  A  better  method 
is  to  forcibly  spray  the  mouth  with  a  1  to  3  per  cent,  solution  of  hydrogen 
dioxide  in  order  to  force  infective  material  from  about  the  teeth.  The 
other  solutions  may  then  be  used.  This  spraying  should  be  somewhat 
prolonged  when  the  mucous  membrane  is  likely  to  be  injured.  Many 
operators  keep  a  stock  of  inexpensive  toothbrushes  for  such  cases, 
which  are  thrown  away  after  the  patient  has  used  them,  who  is  directed 
to  scrub  the  teeth  well  with  brush  and  the  antiseptic  solution. 

The  routine  practice  of  scaling  and  polishing  the  teeth  and  pre- 
scribing an  antiseptic  mouth-wash  prior  to  the  commencement  of  a 
series  of  sittings  is  to  be  highly  commended. 

If  ulcerations  or  inflammatory  conditions  exist,  the  sterilization  is 
to  be  prolonged,  using  such  agents  as  meditrina.  If  a  suspicion  of 
syphilis  exist,  not  only  should  the  mouth  be  freely  washed  with  strong 
antiseptics,  but  special  instruments  should  be  used,  preferably  an  old 
set,  kept  sterilized  and  used  only  in  special  cases.  If  the  hands  of 
the  operator  have  abrasions  or  irritated  spots,  they  should  be  covered 
with  collodion,  and  after  the  operation  should  be  carefully  sterilized 
to  prevent  personal  infection,  of  wliich  a  number  of  cases  have  been 
recorded. 

A  deep  infection  may  usually  be  prevented  during  the  treatment 
of  pyorrhoea  alveolaris  and  pulp  gangrene  by  attention  to  the  steril- 
ization of  the  infected  tract  before  beginning  work  upon  the  parts 
or  during  its  progress-  These  methods  have  been  indicated  in  the 
discussion  of  these  subjects. 


INDEX. 


ABNORMAL  food  supply  as  disease 
cause,  24,  26 

nerve  supply  as  disease  cause,  27 

physical  condition  as  disease  cause, 
27 

waste  products,  effects  of,   27 

remoyal  as  disease  cause,  24-27 
Abnormalities  of  teeth,  206 
Abrasion,  248 

appearance  of,  248 

causes  of,  248,  251 

cervical,  250 

by  clasp,  250 

degrees  of,  248 

eburnation  in,  251 

effects  of,  251 

epithelioma  from   sharp  edges    in, 
251 

fracture  after,   251 

hyperemia  in,   388 

hyperacidity  of  sahva  in,   251 
of  urine  in,  252 

labial,   250 

occlusal,  248 

occurrence  of,  248 

pathology  of,  249 

by  plate,  251 

proximal,  250 

pulp  exposure  from,  252 

rectal  parasites  in,  252 

secondary  dentine  in,  251 

sharp  edges  from,  249,  251 

treatment  of,  252 
Abscess,  acute,  88,  459 

apical,    463.       See    Pericementitis, 
septic. 

blind,  465,  476  - 

causes  of,  81 

definition  of,   88 

dental.      See  Pericementitis,  septic. 

gouty,  579,  580,  584.     See  Perice- 
mental abscess. 

maxillary,  243 

pathology  of,  88 

pericemental,  579.     See  Pericemen- 
tal abscess. 

pointing  of,  89,  464 

of  pulp,  405.     See  Pulp,  abscess  of. 

scars  from  treatment  of,  490 

secondary  to  pyorrhcea  alveolaris, 
556,  576,  586 

with,  fistula,  89,  476,  480 
Accidents  to  teeth,  521.     See  Fracture. 


Acetanihd  as  anodyne,  330,  400,  601 

as  antipyretic,  473 
Acidity  of  mouth,  337 
Acids.      See  modifjdng  adjective — e.  g., 
lactic, 
effect  upon  teeth,    156,    251,    256, 
294,   542 
Aconite,   tincture  of,   as  anod\Tie,   202, 
387,  470 
dental,  470 

to  reduce  heart  action,  80 
Actinomycosis  of  mouth,  614 
Adenoids   as   causes   of   irregularity   of 

teeth,  234 
Adrenalin   chloride,  332,  392,  415,  421, 

456 
Agenesia,  60 

of  enamel,  213 
Agglutination,  33,  49 
Alcohol  as  counterirritant,  201 
as  drier,  331,  345 
as    solvent,     245,    341,    387,    420, 

528 
use  of,  internally,  105 
Alexins,  33,  47 
^Alum,  as  astringent,  569 

as  mummifver,  434,  441 
as  styptic,  392,  400 
Alveolar  necro.sis,   treatment   of,   492 
process,  168 

dependence  upon  teeth,   193 
development  of,  193 
enlargement  of,  134 
hypertrophy  of,  507,  531 
interstitial     inflammation     of, 

530 
necrosis  of,  429,  493,  555 
resorption    of,    250,    530,    532, 
555 
regeneration  of,  578 

surgical  anatomy  of,  168 
Amadou,  use  of,  405,  420 
Amalgam  facing,  use  of,  387,  427 
Amber,  use  of,  264 
Amelification,  124 
Ameloblasts,  118 
Ammonia,  use  of,  337 
Ammonium  carbonate,  use  of,  336 
Ammonol,  use  of,  330 
Amoeba  dysenterise,  35 
properties  of,  18 
structure  of,  18 
Amoeboid  movement,  18 


622 


INDEX. 


Amputation  of  roots  in  acute  abscess, 
473 
in  chronic  abscess,  484 
method  of,  487 
in  perforations,  494,  502 
Amyloid,  437 
Anabolism,  22 
Ansemia,  26,  71 
chlorotic,  73 
debiUty  in,  72,  73 
degeneration  of  cells  in,  74 
htemoglobin  in,  72 
influence  on  caries,  291 

on   pyorrhcea   alveolaris,    551, 
573 
leuka?mic,  73 
pernicious,  74 
symptomatic,  73 
traumatic,  72,  77 
Anaesthesia  of  pulp,  333 
Anaesthetics,  general,   329 

local.    iSee  Cocaine. 
Anatomy,  surgical,  of  teeth,  156 
Ankylosis  of  roots,  509 
Anomalies  of  teeth.    See  Malformations. 

of  number,  230 
Antibacterial  influences,  47,  49 
Antikamnia,  use  of,  330 
Antiphlogistics,  use  of,  473 
AntipjTetics,  use  of,  102,  105,  472 
Antipyrin,  use  of,  601 
Antiseptics  for  blood,  104,  492 
for  canals,  452 
for  ca^dties,  344,  345 
for  mouth,  357,  528,  569 
for  pyorrhoea  pocket,  569 
Antitoxins,  32,  49 

Antrum  of  Highmore,  empyema  of,  481, 
489 
fistula  in,  488 
relations  of,  174,  467,  489 
Aphthae,  607 
Aphthous  ulcer,  607 
Aplasia,  60 

Aqua  regia,  use  of,  433,  438 
Arch,  V-shaped,  234 
Architecture  of  teeth,  166,  436 
ArgA-rol,  use  of,  570 
Aristol.  use  of,  92,  344,  348,  475 
Arsenic  in  cobalt,  440 
iodide,  use  of,  397 
Arsenical  fibre,  425 
Arsenious  acid,  in  abscess  of  pulp,  408 
accidents  with,  429 
action  of,  idiosj-ncrasy  as  to,  425 
upon  gum,  424,  429 
upon  pulp,  422 
variations  in,  425 
application  of,  mode  of,  426 

of,  second,  427 
coverings  for.  426 
dangers  of,  424,  427,  429 
forms  in  which  used,  425 
in  hj^persensitive  dentine,  337 
and  mummif}-ing  paste,  431 


Arsenious  acid,  necrosis  from,  429 
in  nostrums,  430 
passage   of,   through   foramen, 
424,  430 
through  perforation,  431 
pastes,  separation  of,  425 
pocket  for,  400,  428 
poison  from,  428 
in  pulp  nodules,  378 
in  pulpitis,  400 
suffusion  from,  423,  432 
sjTnptoms  from,  429 
in  temporary  teeth,  418,  426 
use  of,  422 

rules  for,  426 
in  venous  hypersemia,  372 
Arterial    hyper£emia,    78.      See   Hyper- 

semia. 
Arteries,  calcification  of,  66,  70 
obstruction  of,  67 
sclerosis  of,  69 
Articulating  paper,  use  of,  516 
Asbestos,  use  of,  345,  352 
Astringents,  use  of,  80,  528,  569 
Atomizer,  use  of,  570 
,  Atony,  60 

j  Atrophy,  causes  of,  61 
I  general,  61 

local,  60 
Attachment  of  teeth,  522 
Autointoxication,  102,  526 


BACILLI,  38 
Bacillus  anthracis  in  blood,  39 

necrodentalis,  394 

pulpse  gangrenae,  346,  450,  461 

tuberculosis,  45,  613 

tj-phosus,  45 
Bacteria,  action  of  gastric  juice  on,  46 
in  media,  41 

predisposition  to,  28,  31,  44 
aerobic,  40 
anaerobic,  40 
in  blood,  39 
classification  of,  37,  38 
cultures  of,  40 
degeneration  of,  39 
facultative,  40 

fermentations  produced  by,  37,  41 
flagella  of,  37 
in  green  stain,  272 
grouping  of,  38 

intestinal  infection  by,  46,  602 
involution  forms  of,  39 
life  conditions  of,  37,  42 
mode  of  entrance  to  body,  39,  602 
monomorphic,  39 
of  mouth,  44 
non-motile,  37 
non-pathogenic,  40 
normal  flora,  42 
obligate,  40,  45 
oral  infection  by,  46,  602 
parasitic,  39 


INDEX. 


623 


Bacteria,  pathogenic,  40 

pleomorphic,  39 

pyogenic,  43,  44,  202,  401,  406,  461 

resistance  of  part  to,  32 

of  tissues  to,  32,  47,  614 

rest  as  factor  in  life  of,  44 

saprophytic,  40 

size  of,  36 

soil  of,  39,  40,  41,  42 

specific,  42 

spores  of,  38 

spreading  of,  in  body,  43 

thenxial  death  point  of,  37 

toxic  action  of,  39 

unorganized  ferments  of,  41 

zooglcea  of,  38 
Bacteriolysis,  33,  49 
Band,  dental,  115 
Bands,  use  of,  268 
Benzoic  acid,  use  of,  528 
Benzoin,  use  of,  245,  392,  399 
Bicuspids,  architecture  of,  166 

eruption  of,  194 

impaction  of,  241 

surgical  relations  of,  173 
Bismuth,  use  of,  190 
Bite,  opening  of,  252 
Black  stain,  272 

Black's  mixture,  use  of,  570,  578 
Blastomycetes,  34 

pathogenic  in  mouth,  602 
Bleaching  processes,  274.  431 
Blindness  from  dental  disease,  508,  599 
Blisters,  use  of,  80 
Blood,  bacillus  anthracis  in,  39 

bacteria  in,  39 

bacterial  enzj-mes  in,  33 

bactericidal  properties  of,  33,  48 

calcium  salts  in,  536,  551 

clotting  of,  74 

coagulability  of  altered,  77 

coagulation  of,  74 

in  capillaries,  68,  74 

ferments  in,  74 

in  inflammation,  84 

corpuscles   in   health   and   disease, 
71 

erj'throblasts  of,  71 

erythrocytes  of,-  71 

germicidal  power  of,  48 

-lettmg,  82,  92,  392,  399 

phagocj'tes  of,  48,  72 

platelets  of,  74 

supply  to  teeth,  152 

urates  in,  552 
Bone,  development  of,  in  jaw,  122,  127 

formation  of,   66 

infection  in  dental  lesions,  491 

inflammation  of,  97 

necrosis  of,  98,  493 

regeneration  of,  100,  488,  578 

suppuration  of,  89 
Borax,  use  of,  189,  528 
Boroglvcerin,  use  of,  528 
Bridge-work,  use  of,  253,  351,  514,  568 


Broaches,  barbed,  432,  438 

broken  in  canals,  438 

Dayton,  497 

Do^Tiie,  432 

Kerr,  432 

pushed  through  apical  foramen,  438 

Swiss.  432,  437,  438 
Bromide  of  potassivmi,  use  of,  601 

of  sodium,  use  of,  161 
Brush,  use  of,  356,  569 

wheels,  use  of,  274,  544 


CAFFEIXE,  use  of,  473,  601 
Calcareous  degeneration,  66 
of  pulp.     See  Pulp. 
Calcification,  122 

after  pus  formation,  89 
of  arteries,  66,  70 
of  dentine,  123 
of  teeth,  129,  133 
of  thrombi,  74 
tubular,  251,  310,  320,  364 
Calcium  chloride,  use  of,  77,  522 
Calcoglobulin,   122,  376 
Calcospherites,  122 
Calculi,  origin  of,  66 
Calculus,  salivan,-,  533 
analyses  of,  535 
in  children,  537 
composition  of,  534 
hardening  of,  540 
mode  of  formation  of,  537 
odor  of,  537 
origin  of,  534 
pathological  effects  of,  541 
pigmentation  of,  537 
progress  of,  542 
recurrence  of,  533 
stratification  of,  534 
treatment  of,  542 
urates  in,  537 
varieties  of,  534 
serumal,  533 

analyses  of,  535 
in  apical  abscess,  477,  482,  548 
hsematogenic,  549 
mode  of  formation  of,  540 
pyogenic,  477,  482,  548,  555 
in  pyorrhoea  alveolaris,  554 
subgingival,  546 
cause  of,  546 
effects  of,  547 
pathology  of,  546 
sjmiptoms  of,  547 
treatment  of,  548 
on  unerupted  tooth,  549,  583 
urates  in,  583 
Calendula,  use  of,  528 
Callahan   method   of   enlarging    canals, 

452 
Calomel,  use  of,  608 
Camphor,  use  of.  337.  399,  570 
Canada  balsam,  use  of,  345 
Canals,  pulp,  accidents  to,  438 


624 


INDEX. 


Canals,  pulp,  broken  broaches  in,  438 
cleansing  of,  432 
continuity  of,  loss  of,  457 
disinfection  of,  452,  470 
enlargement  of,  432,  452,  479 
filling  of,  435 

lining  with  sih-er  nitrate,  453 
Cancrum  oris,  607 
Canker  sore,  607 
Cantharides,  danger  of,  421 

use  of,  421 
Capillaries,  obstruction  of,  67,  531 

thrombosis  of,  74 
Capping  of  pulp,  347 
Capsicum  and  myrrh,  use  of,  200 

plaster,  use  of,  472 
Carbolic  acid  as  anaesthetic,  405 

as  antiseptic,  352,  432,  454,  486 
as  caustic,  189,  415,  421,  422, 

608 
as  ingredient  in  formula-,  245, 

335,  337,  348,  425,  570 
as  obtundent  of  hypersensitive 

dentine,  253,  336 
as  sedative,  387 
Carcinomata,  59 
Caries,  dental,  acids  of,  282,  283 
age  as  factor  in,  290,  320 
alkalies  in,  284 
almost  exposed  pulp  in,  343 
arrangement  of  teeth  in,  287 
bacteria  of,  281,  292,  299,  308 
bodilv  condition  as  factor  in, 

29i 
calcium  salts  produced  in,  258, 

305,  309 
causes  of,  280 
exciting,  280 

general  predisposing,  289 
local  predisposing,  285 
theories  of,  277 
Caush's  tubes  in,  288 
cavity  production  in,  302 
of  cementum,  313 
changes   of   saliva  influencing, 

291 
clinical  historj^  of,  314 
cooked  food  as  factor  in,  284 
decalcification  in,  294,  298,  301 
deep-seated,  339,  341 
defects  of  teeth  in,  286 
destruction  of  dentine  in,  301, 
304 
Nasmvth's  membrane 
in,  301 
diagnosis  of,  322 
diet  in,  285 

enlargement  of  tubules  in,  302 
erosion  and,  256 
exploration  for,  323 
exposure  of  pulp  in,  306,  346 
factors  in,  283 
form  of  teeth  in,  286 
healing  of,  320 
heredity  as  factor  in,  289  i 


Caries,  dental,  history  of,  277 

hvpersensitivitv  of  dentine  in, 

"  325 
including  the  pulp  canal,  457 
in  interglobular  spaces,  307 
leaving  decalcified  dentine  in, 

344 
liquefaction  of  dentine  in,  304 

foci  in,  306 
loss  of  crown  by,  321,  351 

of  root  by, '321 
microbic  placjues  in,  289,  292 
Miller's  experiments  on,  280 
morbid  anatomy  of,  292 
neutralization  of  acid  in,  304 
pathology  of,  292 
pigmentation  in,  312 
prenatal    and    postnatal   influ- 
ences in,  290 
prognosis  of,  325 
Ijrophylaxi's  of,  356 
rapidity  of  progress  of,  318 
recurrence  of,  354 
relative    liability   of   teeth    to, 

316 
secondary,  307 
signs  of,  322 

simple,  treatment  of,  339,  340 
situations  in  which  found,  292 
stages  of,  340 

structure  of  enamel  in,  288,  289 
sugar  and  starches  in,  283 
superficial  treatment  of,  339 
systemic  disease  as  factor  in, 
291 
effects  of,  358 
of  temporary'  teeth,  351 
terminations  of,  321 
therapeutics  of,  340 
transparent  zone  in,  309 
tube  casts  in,  309 
undermining,  319 
variations  in  progress  of,  320 
Cartilage  of  Meckel,  112 
Caseation,  64,  89 
Castor  oil,  use  of,  190 
Catabolism,  22 

Cataphoresis,  introduction  of  drugs  by, 
for  canal  disinfection,  453, 

479,  486 
dangers  in,  429,  430 
for  hypersensitive  dentine, 

332,  341 
irritation    resulting    from, 

389 
for  pulp  removal,  378,  419 
Cathartics  in  dentition,  190,  191 
,  as  derivatives,  80,  400,  470 
Cavitine,  use  of,  342,  343 
Cells,  ama?boid  movement  of,  19 
degeneration  of,  23,  62 
destruction  of  vitality  of,  67,  68 
functions  of,  19 
health  of,  20 
hypertrophy  of,  51 


INDEX. 


625 


Cells,  infiltration  of,  62 
malnutrition  of,  62 
nutrition  of,  19,  22 

interfered  with,  62,  167 
reproduction  of,  19 
sedation  of,  21 
specialized,  22 
stimulation  of,  20 
structure  of,  17 
Cementification,  127 

tables  of,  129,  133 
Cementum,  148 
caries  of,  313 
death  of,  482 
deposition  of,  127 
hypertrophy  of.     See  Hypercemen- 

tosis. 
infection  of,  482 
interdentinal,  130 
malformations  of,  214,  222 
staining  of,  248 
surgical  anatomy  of,  163 
Cervix,  definition  of,  135 
Chalk,  use  of,  190,  264,  338,  544 
Chancre  of  mouth,  611 
Chemical  causes  of  disease,  27 
Chemotaxis,  48,  86 
Ciiloral  hydrate,  use  of,  191,  330 
Chlorine,  use  of,  275 
Chloroform,  use  of,   as  analgesic,   202, 
399,  405 
as  counterirritant,  387 
as  general  anaesthetic,  329 
as  ingredient  in  formulae,  337, 

405,  420 
as  solvent,  264,  399,  405,  435 
in  pulp-pressure  anaesthesia,  420 
Chloro-percha,  use  of,  392,  435,  436,  458 

antiseptic,  437 
Chlorosis,  71,  73 

Chorea  from  hypercementosis,  596 
Chromic  acid,  use  of,  337 
Cinchona  bark,  use  of,  569 
Cingule,  enlarged,  226 
Cinnamon,  oil  of,  discoloration  by,  456 
use   of,   as   ingredient   of   for- 
mula^,    245,     425,     529, 
569,  570 
as  sedative,  387 
Circulation,  22 

local  disturbances  of,  78 
vasomotor  control  of,  78 
Circumscribed  gangrene,  70 
Clasps,  abrasion  by,  250 
Cleansing  of  teeth,  356 
Cleft  palate,  111 

Cloves,  oil  of,  use  of,  as  antiseptic  in 
cavity,  345,  387 
as  canal  antiseptic,  456 
in  hypersensitive  dentine, 

337 
as  ingredient  of  formulae, 
348,  425,  426,  529 
of  pulp  capper,  348 
as  sedative,  387,  399,  415 


Coagulation  of  blood,  74 

in  capillaries,  68,  74 
ferments  in,  74 
in  inflammation,  87 
necrosis,  68 
Cobalt,  use  of,  426,  440 
Cocaine,  use  of,  anaesthesia  by  injection^ 
492,  508,  578,  587 
danger  in,  421 
in  hypersensitive  dentine,  332, 

341 
as  ingredient,  425 
introduced     by     cataphoresis, 

332,  378 
in  pulp  removal,  378,  387,  415, 

419 
as  pulp  sedative,  399 
Cogswell  carrier,  use  of,  274 
Cold  as  a  test,  341,  363,  381,  386,  407, 
445 
as  a  therapeutic  agent,  80,  204,  473 
Colic  in  teething,  184 
Colloid  degeneration,  65 
Colophony,  use  of,  337 
Combinations  of  filling  materials,  use  of, 

343,  352 
Compressed  air,  use  of,  331 
Compresses,  use  of,  77,  203,  204,  473 
Concrescence  of  teeth,  222,  223,  243 
Concussion  of  pulp,  398 
Cone  compound,  234 
Conical  teeth,  216,  231,  234 
Constipation,  effects  of,  588 
Contractility,  18,  21,  23 

stimulation  of,  20 
Comoilsions,  186,  191,  201 
Copper  amalgam,  use  of,  346,  415,  440, 
494 
stains,  269,  273 

removal  of,  275 
sulphate,  use  of,  345 
Cord,  dental,  116 

for  permanent  tooth,  118 
Cork,  use  of,  189 

Corpuscles,  blood,  disintegration  of,  390 
in  health  and  disease,  71 
in  thrombosis,  74 
Cotton,  absorbent,  use  of,  425 
tampon,  danger  of,  491 
use  of,  with  arsenic,  425 

as  a  devitalizing  agent,  422 
in  pulp  removal,  432 
as  a  root  dressing,  437 

filling,  437 
as  a  .test,  346 
Cottonoid,  use  of,  387  * 

Cough  in  teething,  187 
Counterirritation,   use   of,    92,   93,   387, 

400 
Counterpressure  in  pericementitis,  469 
Cows'  milk,  use  of,  192 
Creosote,  use  of,  399,  437 
Crown,  amputation  of,  205,  351 
definition  of,  135 
tool,  use  of,  458 


40 


626 


INDEX. 


Crowning  in  doubtful  cases,  457 

use  of,  219,  252,  268,  350,  353 
Crypts,  dental,   127 
Cultures,  bacterial,  40 
Cuspids,  architecture  of,  166 

eruption  of,  181,   194 

impaction  of,  239 

retention  of  temporary,  198 

supernumerary,  233 
Cusps,  supplemental,  226 
Cysts,  dentigerous,  52,  243 

dermoid,  53 

formation  of,  52 

varieties  of,  52 


DAYTON  broach,  use  of,  497 
Deafness  caused  by  dental  disease, 
508 
Decalcification  of  dentine,  301J 

of  enamel,  271,  294 
Deficiency  of  teeth,  230 
Degeneration,  62 

calcareous,  66,  379 
calcific,  of  pulp,  379.    See  Pulp,  cal- 
cific degeneration  of. 
of  cells  in  ansemia,  74 
colloid,  65 
fatty,  62,  74 
hyaline,  65 
in  inflammation,  87 
lardaceous,"  65 
mucoid,  65 
of  pericementum,  513 
of  pulp,  372,  379 
in  venous  hypercemia,  81 
Dehydrator,  use  of,  331 
Dental  band,  115 

caries,  277.    See  Caries,  dental. 

cord,  116 

crypts,   127 

foUicles,  119,  127,  132 

groove,  115 

pathology,  definition  of,  17 

study  of,  25 
ridge,  115 
Dentinal  changes,  121 
fibrills,  146 
papilla,  117 
tubules,   142 
Dentine,  142 

basis  substance  of,  144 

calcification  of,  123 

caries  of,  301 

changes  -with  age  in,  157 

chemical  composition  of,  157 

decalcification  of,  301 

decalcified,  leaAdng  of,  344,  386,  432 

density  of,  147 

deposition  of,   123 

elasticity  of,  147 

exposed,    reflex    pains    from,    328, 

592 
fibrillar  of,  142 
granular  layer  of,  144 


Dentine,  hypersensitive,  arsenious  acid 
in,  337 
causes  and  pathology  of,  325 
hypersensitivity  of,  325 
diagnosis  of,  329 
in  erosion,  210 
reflex  neuralgia  from,  592 
symptoms  of,  328 
treatment  of,  329 
interglobular  spaces  in,  145 
malformations  of,  213 
physical  properties  of,  157 
recalciflcation  of,  in  caries,  344 
.    repair  of,  266,  397 
resorption  of,  413 
Schreger's  lines  in,  144 
secondarj^,  309,  365 
suffusion  of,  390,  392 
surgical  anatomy  of,  157 
staining  of,  248,  273 
tubular  calcification  of,  364 
tubules  of,  142 
Dentinification,   123 
Dentition,  177 
at  birth,  191 
causes  of  eruption  in,  178 
constitutional  states,  modifying,  191 
first,  177 
hygiene  of,  187 
multiple,  231 
pathological,  first,  182 

constitutional   states   pro- 
ducing, 191 
death  from,  187,  189 
general  symptoms  of,  184 

treatment  of,  189 
intestinal  disturbances  in, 

184 
lancing  in,  187 

hemorrhage  after,  188 
local  symptoms  of,  183 
treatment  of,  187 
nervous    disturbances    in, 

185 
paralysis  in,  187 
puhnonary  disturbance  in, 

187 
reflexes  in,  181,  183,  185 
skin  eruptions  in,  187,  189 
stomatitis  in,  187,  189 
systemic  treatment  of,  189 
second,  199 

convulsions  in,  201 
death  from,  203 
eruption  of  molars  in,  200, 

201,  235 
exanthemata,  influence  of, 

upon,  200 
lancing  in,  201 
stomatitis  in,  201,  203 
symptoms  of,  200 
treatment  of,  200,  203 
.T-rays  in.  198 
periods  of,  186,  194 
process  of,  186,  194 


INDEX. 


621 


Dentition,  second,  193 

disorders  of,   199 
resorption  of  temporary  roots 
in,  195 

symptoms  of,  182 
Depletion,  82,  92,  392,  399,  400 
Derivation  as  therapeutic  means,  80 
Development  of  face  and  jaws,  107 

of  mouth,   107 

of  permanent  teeth,  130 

of  temporary  teeth,  112 
Devitalization  of  pulp,  419 
Devitalizing  fibre,  425 
Diabetes,  influence  of,  on  caries,  291 
Diagnosis,  24 

differential,  24 

direct,  24 

by  exclusion,  24 
Diapedesis,  inhibition  of,  569 

of  leukocytes,  83,  393 

of  red  corpuscles,  81,  390 
Diaphoretics  as  derivatives,  80 
Diathesis,  31 

hemorrhagic,   31,   76 
pathology  of,  77 
treatment  of,  77 
Diet  in  dental  caries,  285 

in  pyorrhoea  alveolaris,  588 
Digestion  of  pulp,  443 
Dilaceration  of  teeth,  224 
Dilatation  of  vessels,   79,   81,   83,  384, 

390 
Disease,  23 

causes  of,  24,  26 
exciting,  26 
predisposing,  28 
proximate,  23 

clinical  history  of,  24 

diagnosis  of,  24 

eti61ogy  of,  24 

functional,  24 

immunity  from,  29.    See  Immunity. 

mode  of  study  of,  25 

morbid  anatomy  of,  24 

previous  disease  as  predisponent  to, 
31 

prognosis  of,  24 

semeiology  of,  24 

therapeutics  of,  25 
Disking  of  teeth,  205,  268,  353 
Dislocation  of  teeth,  521 
Disturbances  of  vascular  system,  71 
Disuse  of  teeth,  516 

results  of,  517 
Diuretics  as  derivatives,  80 
Dobell's  solution,  use  of,  490 
Donaldson's  cleansers,  use  of,  432,  434, 

438 
Downie    broaches,    use    of,    432,    452, 

497 
Drawing  down  teeth,  268 
DriUs,  Beutelrock,  use  of,  497 

broken  in  canals,  438 

Gates-Ghdden,  433,  452 
Dwarf  teeth,  216 


EBURNATION,  251.     See  Transpar- 
ency and  Tubular  calcification. 
Edentulous  mouths,  230 
Electric  mouth  lamp,  use  of,  323,  445, 

488  _  _ 
Electricity  in  dental  therapeutics.     See 
Cataphoresis  and  x-ray. 
effects  of,  on  amoeba,  20 
as  pulp  irritant,  389 
as  test,  408,  445 
Elunination  of  waste,  23 
EmboHsm,  75 
Embolus,  75 

septic,  44,  76 
Empyema  of  antrum  of  Highmore,  481, 

489 
Enamel,  137 

abrasion  of,  248 
absence  of,  212 
agenesia  of,  213 
brittleness  of,  156,  265 
caries  of,  244,  292.    See  Caries,  den- 
tal. 
Caush's  tubes  in,  141 
chalk-like,  213 
chemical  resistance  of,   156 
decalcification  of,  271 
dentinal  processes  in,  208 
deposition  of,  124 
erosion  of,  256 
excrescences,  226 
faulty,  about  sulci,  208 
feel  of,  in  impaction,  244 
fracture  of,  265 
globules,  125,  137,  139 
histology  of,  137 
hyperplasia  of,  212 
interprismatic  cement  substance  of, 

125,  138 
hnes  of  cleavage  in,  265 
malformations  of,  207 
nodules,  225,  226 
opaque  spots  in,  207,  213 
organ,  117 
perfect,  206 

polariscopic  appearance  of,  159 
of  pulpless  teeth,  strength  of,  157 
resorption  of,  254,  512 
rickety,  213 
rods,  137 
solubility  of,  156 
staining  of,  141,  247 
stratification  of,  140,  210 
strife  of  Retzius  in,  210 
striation  of,  210 
stripes  of  Schreger  in,  141 
structure  of,  137 
supplemental  cusps  of,  226 
surgical  anatomy  of,  156 
syphilitic,  212 
transparency  of,  247 
unusual  locations  of,  225 
Encystment  of  teeth,  233,  235 
Endarteritis  obliterans,  531 
Enzymes,  bacterial,  in  blood,  33,  49 


628 


INDEX. 


Epiblast,  products  of,  60 
Epilepsy,  508,  596 
Epithelioma,  56,  59,  255 
Ergot,  use  of,  80 
Erosion,  255 

abrasive  factors  in,  260,  261 
acid  fruits  in,  261 

sodium  phosphate  in,  258 
agency  of  labial  glands  in,  260 
appearance  of,  255 
Baume's  clefts  in,  263 
causes  of,  256 
diagnosis  of,  263 
eburnation  in,  261 
experiments  in,  258,  261 
fracture  in,  262 

hypersensitivity  of  dentine  in,  263 
lactic  acid  in,  258 
location  of,  255 
morbid  anatoiw  of,  261 
periods  of,  263 
polariscope  in,  258 
secondary  dentine  in,  261 
suboxidation  in,  259 
systemic  factor  in,  259,  263 
treatment  of,  263 
lEruption  of  teeth,  177.    See  also  Denti- 
tion, 
causes  of,  178 
difficult,  194 
of  molars,  200,  235 
pathological,  182,  199 
periods  of,  180 
process  of,  180 
symptoms  of,  182,  199 
theories  of,   179 
Eruptive  fevers,  106.    See  Exanthemata. 
Erythroblasts  of  blood,  71 
Erythrocytes  of  blood,  71 
Ether,  use  of,  329,  331,  419 
Ethyl  chloride,  use  of,  331,  363,  415,  419, 

455,  472 
Eucalyptus,  oil  of,  use  of,  337,  528 
Evans'  root  drier,  use  of,  422,  436 
Exanthemata,  effects  of,  on  teeth,  106, 
212 
sequestrum  from,  200 
Excess  of  teeth,  230 
Excretion,  23 
Exfoliation,  68 

Exostosis  of  alveolar  process,  507,  555 
of  tooth  roots.     See  Hypercemen- 
tosis. 
Exploration  for  caries,  323 

for  impaction,  244 
Exposure  of  pulp,  344,  365 
Extension  for  prevention  of  caries,  342 
Extraction  of    hypercementosed  roots, 
508 
indications  for,  191,  198,  204,  244, 
556,  571,  596 
Exudates  of  hypersemia  and  inflamma- 
tion, 81,  390,  395 
Eye,  diseases  of,  caused  by  dental  dis- 
ease, 598 


FACE,  development  of,  107 
Faradic  current,  use  of,  445 
Fatty  degeneration,  62 

of  pulp,  418 
Fermentation,  37,  40 
acetic,  41 
of  albuminous  compounds,  41,  402, 

448 
alcoholic,  41 
lactic,  41 
mixed,  41 

nature  of  products  of,  41     . 
progressive,  41 
Ferments  in  coagulation  of  blood,  74 
organized,  40 
unorganized,  40 
Fever,  100 

oxidation  in,  101 
FibriUse,  dentinal,  146 
Fibrin,  formation  of,  74 
Fibroid  degeneration  of  pericementum, 
519 
of  pulp,  416 
Fibromata,  56 
Fibrosarcomata,  56 
Fistula  in  antrum  of  Highmore,  488 
artificial,  making  of,  471 
on  face,  490 
in  suppuration,  89 
FlageUa,  34,  35,  36 
Fletcher's  carbolized  resin,  use  of,  337, 

350 
Flexion,  224 

Floss  silk,  use  of,  274,  357,  358,  437 
Fluctuation  in  suppuration,  90 
FoUicles,  dental,  119,  127,  132 
Follicular    wall,   development  of,   117, 

121 
Food  supply,  23 

abnonnal,  24,  26 
in  anaemia,  27 
in  circulatory  changes,  27 
Foramen,  large,  treatment  of,  436 
Formagen,  use  of,  345,  348,  387,  444 
in    cavitv    sterilization,    343, 
405      " 
Formaldehyde,  use  of,  in  capping  mate- 
rial, 348 
in  mouth  sterilization,  529 
as  mummifying  agent,  434,  444 
in  canal  sterihzation, 

455 
in    instrument    steril- 
ization,    529,     618, 
619 
in  pulp  suppuration,  408 
Forma-Percha,  use  of,  437,  455 
Fractures  of  teeth,  265 

from  pulp  decomposition,  451 
repair  of,  266,  397 
treatment  of,   267 
Frontal  sinuses,  relations  of,  174 
Functional  disease,  24 
Fungi  as  exciting  cause  of  disease,  34 
Fusion  of  teeth,  220 


INDEX. 


629 


Fusion  of  teeth  by  crowns,  220 
by  roots,  221 
complete,  220 


GALVANIC  shock  of  pulp,  390 
Gangrene,  69 

circumscribed,  70 
dry,  69 
gases  in,  70 
moist,  70 
of  pulp,  444 
dry,  444 
moist,  446 
senile,  69 
sloughing  in,  70 
spreading,  70 
Gases  in  gangrene,  70,  446 
Gastric  juice  as  germicide,  46 
Gates-Glidden  driUs,  433,  439,  497 
broken  in  canals,  438 
Gaultheria,  oil  of,  use  of,  264,  529,  570 
Gauze,  antiseptic,  use  of,  473,  475 
Gelatin,  use  of,  77 
Gemination  of  teeth,  224 
Geranium-fomiol,  use  of,  455 
German-silver  strips,  274 
Giant  cell,  51 
teeth,  216 
Gingival  margin,  136 

resorption  of,  513 
space,  136 
Gingivitis,  interstitial,  529 
causes,  530 
endarteritis  in,  531 
pathology,  530,  555 
resorption  in,  530 
treatment  in,  532 
marginal,  524 

causes  of,  524 
pathology  of,  526 
prognosis  of,  527 
symptoms  of,  526 
treatment  of,  528 
Glands,  pericemental,  153 

of  Serres,  155 
Globules,  enamel,  125 
Glycerin,  use  of,  191,  274,  336,  399,  426, 

441,  443 
Glycosuria,  influence  on  caries,  291 
Glyco-Thymolin,  use  of,  357,  529 
Goldstams,  270 

removal  of,  275 
use  of,  219,  252,  263,  266,  340,  343 
Gonorrhoea  of  mouth,  614 
Gout,  pathology  of,  580 
Gouty  diathesis  and  erosion,  257,  260 
Granular  layer  of  Tomes,  144,  213 
Granulation  tissue,  88,  411,  481,  512 

resorbent  action  of,  483 
Green  stain,  271 

causes  of,  271 
decalcification  under,  271 
removal  of,  274 
Grinding,  use  of,  219,  267,  516 


Grippe  in  antral  empyema,  489 
Griswold  denture,  use  of,  253 
Gritting  of  teeth,  248,  253 
Groove,  dental,  115 
Grooved  teeth,  216,  217,  219 
Guarding  in  pericementitis,  470,  503 
Gum,  atrophy  of,  532 
Giuninata  of  the  mouth,  612 
Gums,  action  of  arsenious  acid  on,  424, 
429 

hypertrophy  of,  415,  427 

inflammation  of.     See  Gingivitis. 

injury  of,  342 

lancing  of,  187,  201 

necrosis  of,  492 

removal  of,  427 

structure  of,  135 

ulceration  of,  204 
Gutta-percha,  use  of,  264,  340,  342,  343, 
345,  350,  352,  388,  436,  440, 
455,  458,  485 
as  root  filling,  435,  488 


HEMOGLOBIN  in  antemia,  72,  73 
iron  in,  73 

solution  of,  81 
Haemophilia,  76,  189 
treatment  of,  77 
Haemostatics,  use  of,  77 
Hair,  relation  to  teeth,  230 
Halisteresis  ossium,  99,  531 
Harelip,  110,  112 
Health,  condition  of,  20 
Heat,  use  of,  as  a  germicide,  49 

as  a  test,  341,  363,  381,  407, 

445 
as  a  therapeutic  agent,  80,  334 
Hemorrhage,   control  of,   77,   392,  400, 

415,  421,  456,  522 
Hemorrhagic  diathesis,  31,  76 
pathology  of,   77 
treatment  of,  77 
infarction,  76 
Herbst's  method  of  treating  pulps,  440 
Hernia  of  pulp,  225,  229 
Histology  of  teeth,  135 
Honeycombed  teeth,  212 
Howship's  lacunae,  215,  244,  397,^530 
Hutchinson's  teeth,  217 
Hyaline  degeneration,  65 
Hydrastis  Canadensis,  use  of,  77 
Hydrochloric  acid,  use  of,  253,  443 
Hydrogen  dioxide,  various  uses  of,  92, 
189,  203,  415,  452,  484,  545, 
577.     See  Pyrozone. 
use  of,  245,  405 
Hydronaphthol,  use  of,  343, 344,  345,  529 
Hygiene,  definition  of,  25 
Hyoscyamine,  use  of,  330 
Hyperaemia,  78,  81 
arterial,  78 

causes  of,  79 
collateral,  78 
compensator}^  79 


630 


INDEX. 


Hypersemia,  arterial,  degrees  of,  79,  385 
enlargement   of   vessels  in,  79, 

38-4 
oxidation  in,  27,  71,  79 
pathology  of,  79 
of  pericementum,  462 
as  predisposition  to  infection, 

79 
of  pulp.    See  Pulp 
reflex,  78 
results  of,  79 
symptoms  of,  79 
treatment  of,  79 
venous,  81 

causes  of,  81 
exudate  of,  81 
pathology  of,  81 
of  pericementum,  517 
of  pulp,  390.    See  Pulp, 
treatment  of,  82 
Hj^percementosis,  243 
causes  of,  505 
diagnosis  of,  507 
neuralgia  from,  596 
paralysis  from,  508 
pathology  of,  506 
results  of,  444 
situation  of,  505 
sjrmptoms  of,  507 
treatment  of,  508 
Hypernutrition,  general  and  local,  50 
Hj^perplasia,  51 
HyperpjTexia,  101 
Hypersensitive  dentine,  325 

arsenious  acid  in,  337 
causes  and  pathology  of,  325 
diagnosis  of,  329 
in  erosion,  263 
reflex  neuralgia  from,  592 
sjTnptoms  of,  328 
treatment  of,  329 
Hypertrophy,  50 

of  alveolar  process,  507,  531 
of  pulp,  411 
Hyphomycetes,  34 
Hj'po-acidity,     general,     influence      on 

caries,  291 
Hyponutrition,  60 
Hypophosphites,  use  of,  397 
Hypoplasia,  60 


iCE,  use  of,  80,  187 
Ichthyol,  use  of,  609 
Idiosyncrasy,  29 
Immune  proteids,  49 
Immunity,  29,  32 
acquired,  32 
to  caries,  285 
Impaction  of  teeth,  235 
caries  in,  244 
cause  of,  240 
diagnosis  of,  243 
exploration  of,  244 
neuralgia  from,  243,  597 


Impaction  of  teeth,  results  of,  243 
symptoms  of,  242 
treatment  of,  244 
under  artificial  denture,  244 
Implantation,  change  of  color  after,  247 
Incisors,  eruption  of,  181,  194 

impaction  of,  241 
Infarct,  hemorrhagic,  76 

of  pulp,  76 
Infarction,  76 
Infection,  mixed,  41,  44 

of  mouth,  602 

prunary,  44 

resistance  of  tissue  to,  47 

after  root  filling,  438 

secondary,  44 
Infiltration  of  cells,  62 

fatty,   62 
Inflammation,  82 

areas  of  involvement  in,  85 

blood  supply  in,  27 

of  bone,  97 

catarrhal,  85 

causes  of,  82 

chronic,  410 

coagulation  in,  84 

degenerations  in,  87 

diapedesis  in,  84 

exudate  of,  81 

fibrinous,  85 

infective,  82 

symptoms  of,  90 

interstitial,   529 

of  alveolar  process,  530 

local  predisposition  to,  90 

oxidation  in,  27,  86 

pathology  of,  83 

phagocytosis  in,  84 

productive,  85 

prognosis  of,  90 

of  pulp,  393 

recumbency  in,  398 

regeneration  after,  93 

resolution  in,  85 

serous,  86 

simple,  82,  479 

symptoms  of,  86 

suppuration  in,  87 

s^miptoms  of,  86,  90 

terminations  of,  87 

treatment  of,  90 

varieties  of,  83 
Injur}^,  mechanical,  of  teeth,  265 
causes  of,  265 
repairs  of,  266 
treatment  of,  267 
Inlays,  use  of,  252,  264 
Innervation,  23 

Insanity  from  dental  disease,  600 
Instillation  method  of  remo-vang  pulp, 

420,  421 
Interglobular  spaces  in  dentine,  145 
Interprismatic  cement  substance,  125 
Interstitial  gingivitis.     See  Gingivitis 
Intoxication,  septic,  102 


INDEX. 


63J 


Intubation  of  root,  use  of,  458 
Iodine,  use  of,  as  aid  in  cleansing  teeth, 
337,  544 
as    counterirritant,    201,    387, 
435,  470  i 

in  pj^orrhoea  alveolaris,  569        i 
as  solvent  of  steel,  438  '• 

Iodoform,    use   of,    92,   345,    348,    426,  : 

454 
Iridio-platinuni,  use  of,  433 
Iron,  chloride  of,  use  of,  472 

stains,  269 
Irritability,  18,  21,  23 
stimiilation  of,  20 
Ischsemia,  71 


JAWS,  development  of,  108 
surgical  anatomy  of,  170 
Jodo-Formagen,  use  of,  345 
Joining  of  teeth,  343 


KARYOKINESIS  of  cells,  19 
Kerr  broaches,  use  of,  432,  452 
Kidneys,  fault}-  elimination  by,  27 
Knife,  tubular,  use  of,  472 
Knocking  out  pulp,  421 
Krameria,  use  of,  528 


LABL\L  abrasion,  250 
glands,  257 

secretion  of,  257 
Lac,  gum,  vise  of,  245 
Lactic  acid,  use  of,  433,  569,  577 
Lacunar  resorption,  99,  397,  530 
Lancing  of  gum,  188,  201,  203 
Lanolin,  use  of,  609 
Lardaceous  degeneration,  65,  66 
Lateral  incisors,  absence  of,  230 
Laudanum,  use  of,  201 
Laxatives,  use  of,  588,  607 
Lead  stains,  270 

use  of,  80,  473 

-water  and  laudanum,  80,  473 
Lemon-juice,  use  of,  192 
Leukseixda,  71,  73 

influence  of,  on  caries,  291 
Leukocytes  in  blood,  71 

amoeboid  movement  of,  2 

phagocytic  action  of,  19,  21,  48,  84, 
87 
Leukocythsemia,  71 
Leukocytosis,  71,  73 

normal  and  pathological,  71 
Lining  ca^dt5r,  345 
Liquefaction  foci,  306 

necrosis,  68 
Listerine,  use  of,  190,  529,  607 
Lithium  salts,  use  of,  588 
Luxation  of  teeth,  521 
Lymphatic    infection     in     abscess,    89, 
'467 


MAGNESIUM  carbonate,  use  of,  569 
Magnesia,   milk  of,  use  of,    264, 
338,  357, 
sulphate  of,  203,  400 
Malaria,  hsematozoon  of,  35 
Malformations  of  cementum,  214 
of  enamel,  206 
dentine,  213 
of  roots,  227 
of  teeth,  206 
Mahgnant  tiomors,  56 
Malnutrition,  60,  62 
Malocclusion  of  teeth,  515 
Malpositions  of  teeth,  233 

causes  of,  234 
Manganese  stains,  269 
Mastication,  force  of  muscles  of,  176 
Maxillte,  development  of,  133 
Maxillarv  periostitis,  243,  474,  483 

abscess,  243,  483 
Mechanical  causes  of  disease,  27 

injury  of  teeth,  265.     See  Injury. 
Meckel,  cartilage  of,  112 
atrophv  of,  112 
Meditrina,  use  of,  405,  453,  470,  587 
Membrane,  Nasnwth's,  142 

pericemental.     See  Pericementum. 
Menthol,  use  of,  341,  387,  392,  399,  405, 

435,  529 
Mercurv,  bichloride,  action  of,  503 
effects  of,  200,  503 
stains  of,  270 

use  of,  49,  105,  92,  203,  357, 
441,  453,  472,  486,  492,  577, 
587 
Mesoblast,  products  of,  60 
MetaboHsm,  22,  23 
Metallic  stains,  269,  273 
Metastasis,  43 

of  tumors,  59 
Microbic  plaques,  292 
Micrococci,  38 

classification  of,  38 
Micro-organisms  as  exciting  causes  of  dis- 
ease, 34 
Mitosis  of  cells,  19 
Molars,  eruption  of,  181,  194 
first,  importance  of,  235 
fourth,  231 
impaction  of,  235 
Monomorphic  bacteria,  39 
Moose-liide  wheels,  use  of,  543 
Morphine,  use  of,  93,  330,  399,  400,  421, 

425,  426 
Motor  disturbances  of  dental  origin,  599 
Mouth,  acidity  of,  337 
actinomycosis  of,  614 
bacteria  of,  44 
chancre  of,  611 
development  of,  107 
gonorrhoea  of,  550,  614 
gummata  of,  612 
infections  of  and  from,  602 
prop,  use  of,  189,  204 
sterilization  of,  452,  474 


632 


INDEX. 


Mouth,  syphilis  of,  609 

steriUzation  in,  620 
syphihtic  affections  of,  609 
tuberculosis  of,  613 
washes,  antiseptic,  338,  528 

Mucin,  coagulation  of,  by  lactic  acid,  538 

Mucoid  degeneration,  65 

Mucous  patches,  612 

Multinucleated  cells,  51 

Multiple  dentition,  231 

Mummification  of  pulp,  441 

Mummif3-ing  paste,  441 

reaction  -wnth  arsenic,  431 

Murexid  test  for  urates,  583 

Muscles,  stiffness  of,  in  dentition,  202 

Mustard,  use  of,  80,  191 

Mycetozoa,  34 

Myrrh,  use  of,  200 


]^ASMYTH'S  membrane,  127,  142 
Xi  caries  of,  301 

Necrobiosis,  68 
Necrosis,  67 

alveolar,  treatment  of,  492 

of  alveolar  process,  429,  493,  555 

of  bone,  98,  429,  493 

from  arsenic,  429 

from  arsenious  acid,  429 

causes  of,  67 

coagulation,  68 

in  eruptive  fevers,  106,  209 

in  inflammation,  87,  97 

Uability  to,  68 

liquefaction,  68 

types  of,  68 
Nerve,  fifth  cranial,  plan  of,  571 

terminals  of,  in  pericemen- 
tum, 153 
in  pulp,  147,  326,  328 
Nerves,  trophic,  27 

vasomotor,  28,  78 
of  pulp,  385 
Nervocidm,  use  of,  334,  341,  415,  421 
Nervous  disorders  of  teething,  185 

disturbances   from   dental   disease. 
See  Reflexes. 

system,  influence  on  disease,  28 
Neuman,  sheath  of,  143 
Neuralgia    about    teeth    from   various 
sources,  596 

caused  by  impaction,  243,  597 

of  dental  origin,  590 

from  hypersemia  of  pulp,  383 

from  hypercementosis,  508,  596 

from  hj^persensitive    dentine,    328, 
592 

from  inflammation  of  pulp,  398,  400 

from  moist  gangrene  of  pulp,  496 

from  pericemental  disease,  595 

from  pulp  disease,  594 
nodules,  376,  378 

reflex,  from  hj'persensitive  dentine, 
592 

from  root  resorption,  513 


Neuralgia,  treatment  of,  60 

from  use  of  arsenic,  429 
Neuroses,  reflex.    See  Reflex  pains. 
Nickel  stains,  270 
Nitric  acid,  use  of,  253,  337,  438 
Nitrous  oxide,  use  of,  400,  419 
Nodules,  cemental,  215 

enamel,  226 

pulp.     See  Pulp  nodules. 

effect  of  arsenic  in  cases  of,  378 
Noma,  91,  608 
Non-conductors,  use  of,  341 
Nucleases,  49 
Nuclein,  33 

Nucleus,  diA'ision  of,  20 
Number,  anomalies  of,  230 
Nutrition,  alteration  of,  23 

of  ceUs,  22 

disturbances  of,  50 

excess  of,  50 

deficienc}^  of,  60 

impaired,  67,  72 


OBTUNDENTS  of  hypersensitive  den- 
tine, 329,  330 
of  pulp  pain,  387,  399,  405,  408 
Occlusal  abrasion,  248 
Occlusion,  loss  of,  248,  515 

of  teeth,  167,  175 
Odontitis  infantum,  183 
Odontoblasts,  146,  194 

appearance  of,  121,  123,  144,  146 

arrangement  of,  121,  123,  146 

atrophy  of,  367 

development  of,  121 

effect  of  stunulation  of,   162,   251, 

261,  310,  364,  365 
function  of,  123 

relations  of,  with  nerve  terminals, 
147,  328 
with  Tomes'  fibres,  146 
Odontoclasts,  194,  214 
Odontomes,  228 
(Edema,  81,  84,  390 
Oidium  albicans,  603 
Oils.     See  qualifj-ing  terms,  e.  g.,  Cloves, 

oil  of. 
Oligocythsemia,  71 
Opium,  use  of,  77,  80,  190,  202,  473 
Orange  wood,  use  of,  274,  421,  559 
Organs,  nature  of,  22 
Orthoform,  use  of,  492 
Ossification,  127 
Osteitis,  98 

Osteodentine,  371,  397 
Osteomalacia,  531 
Osteomyehtis,  98,  491 
Osteoporosis,  98 
Osteosclerosis,  98 

Ovary,  pain  in,  from  dental  disease,  599 
Overuse  of  teeth,  513 

pathology  of,  514 
treatment  of,   514 
Oxalic  acid,  use  of,  452 


INDEX. 


633 


Oxidation  of  cells,  20-26 

increased,  51 

ia  fever,  101 

heat  due  to,  23,  86 

va.  hypersemia,  79,  81 

in  inflammation,  86 

lessened,  60 
Oxygen,  nascent,  452 

importance  of,  to  tissues,  20,  22,  63, 
81 


PALATE,  cleft,  HI 
Papain,  use  of,  443 
Papilla,  dentinal,  117 

changes  in,  121 
Paraffin,  use  of,  436,  475 
Paraform,  use  of,  349,  436 
Paralysis  from  dental  disease,  599 
from  hypercementosis,  508 
of  vessels,  392 
Parasitic  bacteria,  39 
Paste,  arsenical,  425 
Kowarska's,  562 
mummifying,  441 
Patches,'"mucous,  612 
Pathogenic  bacteria,  40,  42 
Pediluvium,  hot,  93,  470 

as  a  derivative,  80,  204 
PeniciUium,  35 
Peppermint,  use  of,  528,  569 
Perforating  canal  resorption,  100 
Perforation  by  caries,  349,  415 
treatment  of,  349 
by  driU,  415,  435 

treatment  of,  436 
exostosis  following,  507 
by  resorption,  511 
Pericemental  abscess,  461,  468,  483,  579 
causes  of,  579 
diagnosis  of,  586 
general  pathology  of,  580 
morbid  anatomy  of,  584 
prognosis  of,  587 
special  pathology  of,  582 
symptoms  of,  584 
treatment  of,  587 
glands,  153 
Pericementitis,  459 

acute  septic  apical,  460 

causes  of,  460 
clinical  history  of,  465 
complicated    by    per- 
foration, 494 
confluence  of  cachexia 

in,  467 
diagnosis  of,  468 
direction  taken  by  pus 

in,  464 
extraction  in,  474 
necrosis  in,  475,  493 
pathology  of,  462 
prognosis  of,  469 
septic  intoxication  in, 
465 


Pericementitis,  acute  septic  apical,  stages 
of  pus  formation  in, 
463 
streptococcal       infec- 
tion in,  465 
symptoms  of,  459,  462 
treatment  of,  469 
systemic,  472 
use    of    poultices    in, 
467 
aseptic.      See   Pericementitis,  non- 
septic, 
chronic  septic  apical,  with  blind  ab- 
scess, 498 
with  fistula,  480 

destruction  of  tis- 
sue in,  477 
diagnosis  of,  483 
direction  of    pus 

in,  481 
discharging  exter- 
nally, 490 
healing  of,  480 
pathology  of,  480 
symptoms  of,  483 
in    temporary 

teeth,  495 
treatment  of,  484 
without  fistula,  476 
diagnosis  of,  478 
prognosis  of,  479 
sj'mptoms  of,  477 
treatment  of,  479 
non-purulent,  495 
causes  of,  495 
diagnosis  of,  497 
pathology  of,  495 
treatment  of,  497 
gouty.    See  Pericemental  abscess, 
mercurial,  503 
non-septic,  chronic,  504 
results  of,  504 
symptomatic,  503         ^^ 
traumatic,  499 
causes  of,  499 
diagnosis  of,  502 
pathology  of,   501 
prognosis  of,  502 
prophylaxis  of,  501 
sjrniptoms  of,  502 
treatment  of,  502 
Pericementiun,  150 

apical  irritation  of,  407 
as  avenue  to  deep  infection,  520 
bloodvessels  of,  152 
degeneration  of,  513,  516,  517 

fibroid,  519 
diseases  of,  459 

beginning  at  apex,  460 
classification  of,  459 
epithehum  in,  153 
evidence  of  disturbance  of,  459 
fibres  of,  151 

fibroid  degeneration  of,  519 
functions  of,  151 


634 


INDEX. 


Pericementum,  hvperajmia  of,   arterial, 
462 
A-enous,  of,  517 
infection  of,  456,  461 
inflammation  of.     See  Pericementi- 
tis, 
as  a  ligament,  150,  165 
nerves  of,  153 
origin  of,  130 
overuse  of,  514 
structures  in,  152,  155 
surgical  anatoniy  of,  163 
thickening  of,  497 
Periostitis  accompanving  apical  abscess, 
467,  474,  483" 
forms  of,  97 
maxillary,  243 
Permanent  tooth,  development  of,  130 
eruption  of,  194 
^     origin  of,  118 
Phagedenic  pericementitis,  572 
Phagocytosis,  19,  21,  48,  84,  87 
Phenacetin,  use  of,  330,  400,  601 
Phenol-camphor  (campho-phenique),  455 
as  canal  disinfectant,  455 
disinfectant  in  pyorrhoea  pock- 
ets, 570,  578 
formula  for,  570 
in  hypersensitive  dentine,  337 
as  obtundent  of  pain  in  tissues, 

492 
in  pulp  diseases,  387,  399 
-sodique.  use  of,  189,  200,  357 
Phosphaturia,  536 
Phj'-sical  condition,  abnormal,  24,  27 

as  disease  causes,  27 
Pigmentation  in  caries,  312 
Pilocarpine,  action  of,  504 
Piscidia  ervthrina,  use  of,  330 
Pitted  teeth,  216,  219 

treatment  of,  219 
Plantations,  result  of,  511 
Plants,  classification  of,  34 
Plaques,  microbic,  292 
Plaster  of  Paris,  use  of,  348 
Plates,  use  of,  253,  351 
Pleomorphic  bacteria,  39 
Plethora,  50,  71 
Pocket  for  arsenic,  427 
Pointing,  89,  90 

Poisons,  effect  on  protoplasm,  26 
Polycji;h3emia,   71 
Polypi  as  causes,  234 
Porcelain,  use  of,  219,  340,  560 
Potassium  bromide,  use  of,  601 
carbonate,  use  of,  336 
chlorate,  use  of,  189 
hydrate,  use  of,  335,  452 
iodide,  action  of,  504 
permanganate,  use  of,  452 
Potassocain,  use  of,  332 
Poxiltices,  use  of,  467,  473 
Powder,  tooth,  use  of,  357,  569 
Predisposition  to  action  of  bacteria,  28, 
31,  44,  45,  79 


Pregnane}-,  influence  of,  on  alveolar  re- 
sorption, 531 
on  caries,  291 
causing  reflexes  to  teeth,  601 
Pressure  anaesthesia,  dangers  of,  421,  430 
use  of,  400,  405,  415,  419,  420 
Previous  disease  as  predisposing  cause, 

31 
Probe,  magnetized,  use  of,  438 

use  of,  347,  392,  483 
Process,  alveolar,  168 

dependent  upon  teeth,  193 
enlargement  of,  134 
surgical  anatomy  of,  168 
Prophj'laxis  of  caries,  355 

in  pyorrhoea  alveolaris,  558,  569 
in  systemic  disease,  358 
Proteids,  composition  of,  18 

immune,  49 
Protoplasm,  effect  of  poisons  upon,  27 
of  retained  waste  upon,  27 
ph5'siology  of,  21 
structures  of,  18 
Protozoa,  34 
Pseudopodia,  18 

of  amoeba,  18 
Ptomaines,  toxic  and  non-toxic,  42 
Pulp,  145 

abscess  of,  372,  405 

arsenious  acid  in,  408 
diagnosis  of,  407 
pathology  of,  405 
pericemental  irritation  in,  407 
prognosis  of,  408 
sjonptoms  of,  406 
treatment  of,  408 
absence  of  lymphatics  in,  148 
action  of  arsenious  acid  on,  422 
almost  exposed,  343 
atrophy  of,  367,  371 
calcific  degeneration  of,  379,  396  ^ 
causes  of,  379 
pathology  of,  379 
.sj-mptoms  of,  380 
canals,  cleansing  of,  432 
capping,  268,  347,  348,  365,  387 
ca^dties,  shapes  of,  162 
concussion  of,  398 
death  of,  tests  for,  445 
degeneration  of,  372,  379 
fatty,  417,  418 
fibroid,  416 
devitalization  of,  388,  419 

in  impaction,  243 
digestion,  435,  443 
diseases  of,  361 

constructive,  364 
destructive,  382 
symptomatology  of,   362 
in  temporary  teeth.  418 
electric  irritation  of,  389 
exposure  of,  344,  346,  365 
diagnosis  of,  346 
therapeutics  of,  346 
treatment  of,  347 


INDEX. 


635 


Pulp,  fractures  of  teeth  from  decompo- 
sition of,  451 
fungoid,  411 
galvanic  shock  of,  390 
gangrene  of,  444 
dry,  444 

treatment  of,  446 
moist,  446 

causes  of,  447 
discoloration  from,  449 
doubtful  cases  of,  457 
pathology  of,  448 
sjanptoms  of,  450 
treatment  of,  451 
hernia,  225,  229 
hypersemia  of,  arterial,  382 
causes  of,  382 
degrees  of,  385 
diagnosis  of,  385 
idiopathic,  388 
pathology  of,  384 
prognosis  of,  385 
symptoms  of,  383 
treatment  of,  386 
venous,  390 

causes  of,  390 
pathology  of,   390 
prognosis  of,  392 
sjTnptoms  of,  392 
treatment  of,  392 
hypertrophy  of,  411 
infarction,  76 
inflammation  of,  393 
acute,  394 
causes  of,  393 
chronic,  410 

hypertrophic,  411 

diagnosis  of,  414 
epithelium  of,  412 
nerves  in,  412 
pathology  of,  411 
resorption  of  dentine 

in,  413 
treatment  of,  415 
pathology  of,  395 
resolution  in,  396 
resorption  of  dentine  in,  397 
diagnosis  of,  399 
prognosis  of,  399 
sj-mptoms  of,  397 
treatment  of,  399 
mummification,  434,  441 
nodules,  372 

deposition  of,  375 
diagnosis  of,  378 
occurrence  of,  372 
pathology  of,  374 
symptonas  of,  376 
treatment  of,  378 
osteodentine  in,  371 
partial  death  of,  450 

extirpation  of,  440 
puncturing  of,  392 
removal  of,  432 

methods  of  preparation  for,  419 


Pulp,  sclerosis  of,  410 

treatment  of,  411 
sterilization  of,  399,  405 
suppuration  of,  401 
causes  of,  401 
pathology  of,  401 
surgical  anatomy  of,  161 
ulceration  of,  402,  457 
hypertrophy  in,  414 
pathology  of,  402 
phases  of,  404 
sjrmptoms  of,  404 
treatment  of,  405 
vessels  and  nerves  of,  146 
■\dtalitv  of,  tests  for,  445 
Pulpitis,  393.    See  Pulp, 
arsenious  acid  in,  400 
chronic     hvpertrophic,     411.       See 
Pulp. 
Pumice,  use  of,  274,  358,  545 
Puncture  probe,  422 
Puncturing  of  pulp,  use  of,  392,  399,  405, 

407,  408 
Pus,  87 

burrowing  of,  464,  481 
calcification  after,  89 
caseation  of,  89 
causes  of,  43 
pointing  of,  89 
varieties  of,  90 
Putrefaction,  41,  402 

,  of  pulp,  448 
Pysemia,  43,  76,  105 

of  dental  origin,  203,  465,  492,  615 
Pyocyaneo-protein,  use  of,  493 
Pyogenic  bacteria,  43.     See  also  the  sup- 
purative diseases. 
Pj'orrhoea  alveolaris,  550 

begmning  as  a  gingivitis,  553 

bridge-work  in,  568 

catarrh  of  mouth  in,  556 

causes  of,  550,  573 

clinical  division  of  cases  of,  553 

history  of,  554 
dental  caries  associated  with, 

557 
diagnosis  of,  557,  576 
factors  in,  553 
gingival  abscess   secondary  to, 

556 
heteroplasty  after  amputation 

for,  560 
infection  in,  550 
local  origin  of,  552 
odor  in,  556 
pathology  of,  554,  573 
phagedenic,  prognosis  of,  577 
treatment  of,  577 
varieties  of,  572 
prevention  of  mobility  in,  562 
prophjdaxis   of,  558,  569,  571, 

578 
syphilis  in,  550 
systemic  effects  of,  572,  586 
splints  for,  562 


636 


INDEX. 


Pyorrhcea  alveolaris,  symptoms  of,  554, 
57G 
treatment  of,  558.  577 
medicinal,  569  588 
Pyrozone,  25  per  cent.,  274,  415,  421, 
438,  453,  456,  479,  486,  558 


Q 


UININE,  use  of,  400,  472,  473,  569 


RACHITIS,  effect  of,  upon  dentition, 
192 
upon  enamel,  213 
Radiographs.     See  .r-rays,  use  of. 
Red  stains,  273 
Reflex  action,  78 
hj'persemia.  78 

neuralgia  from  hvpersensitiA-e  den- 
tine, 592 
pain,  362,  371,  377,  383 
dental,  590 

from  cliseases  of  the  pericemen- 
tum, 595 
from  exposed  dentine,  592,  595 
facial,  origin  of,  593,  598 
from  general  diseases,  590 
hj^pothesis,  explanatory  of,  595 
location  of,  593,  594 
from  pulp  diseases,  594 
referred  to  teeth,  600 

to  tracts  not  suppUed  by 
fifth  nerve,  598 
treatment  of,  601 
Reflexes,  motor,  of  dental  origin,  599 
Refrigeration,  use  of,  331 
Regeneration,  93.    See  also  Granulation 
tissue, 
forms  of,  93-96 
Removal  of  pulp,  419.     See  Pulp. 
Replantation  of  teeth,  488,  494,  502 
Reproduction  of  cells,  19 
Resorbent  organ,  195 
Resorption,  96 

of  alveolar  process,  243 
of  bone,  96,  530 
of  dentine,  413 
of  enamel,  255 
by  halisteresis  ossium,  99,  531 
lacunar,  99,  530 
perforating  canal,  99,  530 
of  permanent  roots,  509 
causes  of,  509 
diagnosis  of,  512 
idiopathic,  511 
pathology  of,  511 
symptoms  of,  512 
treatment  of,  513 
by  pulp,  196,  397 
of  roots  in  impaction,  243 
of  temporary  teeth,  194 
Rest,  employment  of,  77 

surgical,  use  of,  79,  470,  503 
Retention  of  temporary-  teeth,  198 


Retzius,  striff  of,  140 
Ridge,  dental,  115 

Robinson's  remedy,  use  of,  253  335,'338 
Root,  amputation  of,  473,  484,  487 "  { 
ankylosis  of,  509  \,\ 

apex,  amputation  of.    See  Amputa- 
tion, 
definition  of,  135 
disinfection,  452,  470 
drier,  use  of,  422,  436,  454 
filling,  435,  452,  455,  480 
absorbable,  475 
immediate,  452 
infection  after,  438 
removable,  436,  455 
removal  of,  497 
in  temporarj'^  teeth,  475,'^495 
tentative,  456,  479 
formation  of,  127 

of  permanent,  197 
table  of,  129 
incomplete,  268 
intubation,  458 
long  and  short,  227 
malformations  of,  227 
multi,  fonnation  of,  228 
perforation.     See  Perforation, 
resorption  of,  paralj-sis  from,  596 
of  temporarj'^,  194 
failure  of,  230 
Rose  geranium,  oil  of,  use  of,  569 

oil  of,  use  of,  264 
Rubber  cups,  use  of,  274,  544 

-dam,  use  of,  386,  387,  426,  470 
vulcanite,  use  of,  405,  420,  421,  485 


SACCHARIN,  use  of,  245,  528 
Saccharomyces,  35 
Sacs,  tooth,  127 
Salicylic  acid,  use  of,  528 
Saliva,  analysis  of,  535 

changes  in  composition  of,  291,  545 

551 
hyperaciditj'  of,  in  abrasion,  251 
Salivary  calculus,  533 

analyses  of,  535 

in  children,  537 

composition  of,  534 

hardening  of,  540 

mode  of  formation  of,  537 

occurrence  of,  533 

odor  of,  537 

origin  of,  534 

pathological  effects  of,  541 

pigmentation  of,  537 

progress  of,  542 

stratification  of,  534 

treatment  of,  542 

urates  in,  537 

varieties  of,  534 
Salol,  use  of,  105,  190,  472 
Salve,  antiseptic,  104 
Saprgemia,  103 
Saprophytic  bacteria,  40 


INDEX, 


637 


Sarcomata,  56 

Scalers  for  calculi,  543,  547,  578 

Scar  on  face,  operation  for,  490 

Schizomycetes,  34,  36 

Schreger,  lines  of,  in  dentine,  144 

in  enamel,  141 
Schrier's  aUoy,  use  of,  452 
Sciatica  from  dental  disease,  599 
Sclerosis  of  bone,  98 

of  pulp,  410.     See  Pulp. 
Screws,  use  of,  252,  268,  351 
Scurvy,  infantile,  192 
Secondary  caries,  307 
dentine,  309,  364 

in  abrasion,  251,  369 
causes  of,  364 
in  erosion,  261 
as  obstacle,  371,  408 
pathology  of,  367 
results  of,  371,  381 
Secretion,  19 

stimulation  of,  20,  23 
Sedation  as  a  means  of  treatment,  80, 

387_ 
Sedative  effect  on  cells,  21 
Semeiology  of  disease,  24 
Senile  gangrene,  69-70 
Senility,  effect  of,  upon  caries,  290 
upon  gums,  532 
upon  pericementum,  519 
Septic  disease  of  dental  origin,  614 
infection,  103,  105 
intoxication,  102,  358,  492 
Septicemia,  90,  103,  358,  492 

prevention  of,  472 
Sequestrum,  68 

from  exanthemata,  200 
froni  mercurj^  200 
Serres,  glands  of,  155 
Serum,  blood,  germicidal  properties  of, 
47 
therapeutics,  33 
Sharpey's  fibres,  149 

in  cementum,  149 
Sheaths  of  Neumann  in  dentine,  143 
Shock,  galvanic,  390 

nervous,  354 
Sialosemeiologv  as  diagnostic,  545,  551 
Silk  floss,  use  of,  357,-  358 
Silver,  Crede's  soluble,  105 

nitrate,  use  of,  336,  352,  415,  453, 

479,  488 
ointment,  104 
Sizes  of  teeth,  215 
Skin  eruptions  in  teething,  187,  189 
Sloughing,  70 

Sodiima  bicarbonate,  use  of,  336,  559 
borate,  use  of,  529.    See  Borax, 
bromide,  use  of,  191 
chloride,  use  of,  438 
dioxide,  action  of,  452 

use  of,  49,  343,  379,  438,  484 
hydrate,  use  of,  335,  344 
and  potassium,  allo}^  of,  452 
Specific  bacteria,  42 


Sphacelus,  70 
Spirilla,  38 
Splints,  use  of,  254 
Sponge  graft,  436,  440 
Spores  of  bacteria,  39 
Spunk,  use  of,  405,  420,  427 
Stains,  amalgam,  273 

black,  272 

bleaching  of,  274,  275 

cadmium,  273 

copper,  269,  273 

of  dentine,  273 

gold,  270 

green,  271 

iron,  269,  273 

lead,  270 

manganese,  269,  273 

mercury,  270 

metallic,  269,  273,  275 

nickel,  270,  273 

non-metallic,  271,  275 

red,  273 

silver,  270,  273 

of  suffusion,  274,  390,  392 

tobacco,  272 

treatment  of,  274 
Starch  paste,  use  of,  191 
Starches  as  factors  in  dental  caries,  284 
Stasis  in  inflammation,  84 
Stellate  reticulum,  120 
Steresol  varnish,  use  of,  245,  587 
Sterilization  of  cavity,  343 

dental,   615 

of  dental  apparatus,  617 
of  field  of  operation,  619 
of  hands,  616 
of  rubber-dam,  618 
Stimulation,  effect  on  cells,  20 
Stomach,  effect  of  caries  iipon,  358 
Stomatitis,  604 

catarrhal,  605,  606 

causes  of,  604 

infective,  605 

simple,  605 

sjTnptomatic,  606 

in  teething,  183,  189,  192 

ulcerative,  526,  527,  606 

varieties  of,  604 
Strata  in  enamel,  140 
Stratum  granulosum,  144 

intermedium,  119 
Streptococcus  antitoxin,  use  of,  105 
Strise  of  Retzius,  140 
Strips,  German-silver,  use  of,  274 
Structural  disease,  24 
Struma,  effect  of,  upon  dentition,  192 
Strychnine,  use  of,  105 
Styptics,  use  of,  77,  392,  400,  415,  421 
Subgingival  calculus.     See  Calculus. 
Suboxidation,  diseases  of,  259,  525,  580 
Suffusion  of  teeth,  390,  392,  423,  428 

treatment  of,  432 
Sugars  as  factors  in  dental  caries,  284 
Sulphomethaemoglobin    in  green   stain, 
272 


638 


INDEX. 


Sulphuric  acid,  use  of,  77,  253,  276,  379 

433.  438,  497,  559,  569 
Supernumerary  teeth,  231 
Suppression  of  teeth,  230 
Suppuration,  87 

of  bone,  97 

causes  of,  90 

leukocytosis  in,  73 

of  pulp.    See  Pulp. 

septic£emia  from,  90 

spreading,  89 

symptoms  of,  90 

treatment  of.     See  Suppurative  dis- 
eases, 
by  pvocvaneo-protein,  493 
Swab,  root,  437  " 
Swelling,  cloudy,  64 

as  symptom.     See  Inflammation. 
Swiss  broaches,  use  of,  432,  437,  438, 

453,  497 
Symptomatic  anaemia,  73 
Syphilis,  106,  609 

diagnosis  of,  611 

effects  of,  106,  191,  212,  216,  217 
upon  dentition,  192 
upon  teeth,  106,  504 

hereditarj^,  .signs  of,  219 

of  mouth,  610 

sterilization  in,  620 

personal  infection  by,  617,  620 

primary,  610 

reflex  pains  from,  600 

secondary,  611 

tertiary,  612 
Syphilitic  teeth,  212,  217 
Syringe,  abscess,  485 


TALC,  use  of,  189 
Tannin,  use  of,  336,  434,  444 
Tape,  use  of,  274 
Tartar,  cream  of,  use  of,  569 
Teeth,  abrasion  of,  248 

anomalies  of  number  of,  230 

architecture  of,  166 

articulation  of,  175 

attachment  to  bone,  151.     »See  An- 
kylosis. 

blood  supply  to,  152 

caries  of,  278 

concrescence  of,  222 

conical,  216 

development  of,  106,  112 

diagnosis  of,  176 

diseases  of  pericementi  of,  459 
pulps  of,  361 

dwarfed,  216 

encystment  of,  235 

erosion  of,  255 

eruption  of,  177.     See  Dentition, 
permanent,   193 

exanthematous,  212 

fusion  of,  220 

gemination  of,  224 

giantism  of,  216 


Teeth,  histology  of,  135 

Hutchinson,  217 

impaction  of,  235 

influence  of  feeding  upon,  290,  359 

injury  of,  265 

inspection  of,  235 

malformations  of,  206 
of  roots  of,  227 

malocclusion  of,  515 

malposition  of,  233 

as  mechanical  appliances,  166 

occlusion  of,  174 

pitted  and  grooved,  216,  217 

relations  of,  156 

stains  on,  270 

surgical  anatomy  of,  156 

transparency  of,  309 

variation  in  size  of,  216 
Teething,  29.     See  Eruption   and  Den- 
tition. 
Temperature,  effect  of,  on  cells,  21,  23 
Temporary  teeth,  caries  of,  351 
eruption  of,  181 
moist    gangrene    of    pulps  of, 

457 
pulp  capping  in,  418 
diseases  of,  418 
retention  of,  198,  235 
Teratomata,  53 
Thallophytes,  34 

Thermal  changes,  effects  of,  326,  341 
363,  365,  377,  381,  383,  407 

tolerance,  rate  of,  388 

tests  for  pulp  vitality,  445 
Thirst,  treatment  of,  77 
Thrombosis,  74,  75 

in  pulp,  391,  405 
Thrombus,  74 

hardening  of,  75 

septic,  44,  76 
Thrush  fungus,  development  of,  602 
Thumb  sucking,  235 
Thymol,  use  of,  341,  387,  392,  399,  400, 

405,  408,  426,  441,  529 
Tic  douloureux  from  pulp  nodules,  378, 

599 
Tissues,  22 

analysis  of,  22 

gramilation  of,  88 

nutrition  of,  22 

resistance  to  bacteria,  47 
Tobacco  in  abrasion,  248,  253 

stains,  250,  273,  274 
Toes,  pain  in,  from  dental  disease,  599 
Tolu,  use  of,  245 
Tomes,  granular  layer  of,  144 
Tonics,  use  of,  472 
Toxsemia,  42,  46,  90,  91,  102, 

drug,  102 

intestinal,  102 
Toxins,  32,  39,  42,  49,  90 
Transparent  zone,  309 
Transplantation  of  teeth,  488 

u.se  of,  351 
Traumatic  ansemia,  72,  77 


INDEX. 


639 


Traumatic  pericementitis.     [See  Perice- 
mentitis, non-septic. 
Trephine,  use  of,  471 
Trichloracetic  acid,  use  of,  350,  415,  428, 

558,  569,  577 
Trismus  from  dental  disease,  599 

muscular,  in  dentition,  202 
Trophic  nerves,  27 
Tube  casts,  309 

Tuberculosis,  effects  of,  upon  dentition, 
192 

of  mouth,  613 
Tubular  calcification,  364 
Tubules  of  dentine,  142 

calcification  of,  309,  364 

of  enamel,  141 
Tumors,  carcinomatous,  59 

classes  of,  55 

definition  of,  53 

formation  of,  53 

malignant,  56 

sarcomatous,  56 
Turkish  baths,  use  of,  588 
Twin  teeth,  224 


ULCER,  aphthous,  607 
caused  by  jagged  teeth,  251,  613 
definition  of,  88 
syphilitic,  612 
Ulceration,  89,  91 

of  pulp,  402.     See  Pulp. 
Urates  in  blood,  580 

in  connective  tissue,  581,  582 
deposition  of,  conditions  of,  581 
in  deposits  on  teeth,  583 
elimination  of,  585 
in  joints,  580 
Urea,  origin  of,  23 
Uric  acid,  origin  of,  23,  581 
Urinalysis  as  diagnostic,  545,  551 
Urine,  hyperacidity  of,  in  abrasion,  252 
Uterus,  pain   in,   from  dental    disease, 

599 
Uvula,  cleft.  111  . 


VACCINATION,  33 
Vapocain,  use  of,  332 
Varnish,  amber,  use  of,  264 
benzoin,  399 
in  cavities,  342,  345,  399 
steresol,  245,  587 
Vascular  system,  disturbances  of,  71 

nerves  controlling,  78 
VasoiTiotor  nerves,  78 
Vein,  obstruction  of,  67 

thrombosis  in,  74 
Velum  palati,  cleft.  111 
Venous  hyper£emia,  81 

arsenious  acid  in,  372 


Venous  hypera?mia,  degeneration  in,  81 

exudate  of,  81 

of  pulp,  390 

treatment  of,  81 
Veratrine,  use  of,  202 
Vessels,  dilatation  of,  79,  81,  83,  384, 
390,  392 
paralysis  of,  392 
Vicious  circle,  28,  62 
Vulcanite  rubber,  use  of,  405 


WASH,  mouth,  antiseptic,  528 
Waste  elimination,  23 

products,  eltminative   treat- 
ment of,  571,  588 
retained,  effect  of,  27 
synthesis  of,  23 
removal,  23 

abnormal,  24,  27 
Water,  boUing,  as  germicide,  518 
distilled,  use  of,  276 
as  a  therapeutic  agent,  570,  588 
Wax  as  root  filling,  435,  436,  475 
Wounds,  healing  of,  93-96 


X-RAY,  use  of,  in  diagnosis  of  condi- 
tion of  pulp,  415,  446 
of  hj'percementosis,   508 
of  impaction,  244 
of  odontomes,  229 
of  perforations,  415,  494 
of  pulp  nodules,  378 
in  pyorrhoea  alveolaris,  570 
of  resorptions,  195,  196,  513 
in  treatment  of  neuralgia,  601 
of  pyorrhoea  alveolaris,  555, 
560,  570 


ZINC  chloride,  as  astringent,  528 
effect  of,  upon  cotton,  437 
use  of,  253,  334,  341,  421,  486 
oxide,  use  of,  348,  426,  441 
oxychloride,    in    canal   filling,    435, 
436,  437,  440 
as  cause  of  gangrene,  444 

of  secondary  dentine,  365 
in  deep  decay,  345 
in  fractures,  268 
hydrated,  use  of,  345 
oxyphosphate  in  canal  filling,  436 
in  deep-seated  caries,  342,  343, 

348 
in  erosion,  264 
in  fractured  teeth,  268 
in  hyperemia  of  pulp,  387 
as  support  to  enamel,  266 
oxysulphate,  use  of,  334,  348 
Zoogloea  of  bacteria,  38 


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